The fuel fabrication facility has been built and is being operated by KAERI since licensing research reactor fuel fabrication in 2004. After almost 20 years of operation, outdated equipment for fabrication or inspection has been replaced by automated, digitalized ones to assure a higher quality of nuclear fuels. However, the generation of a large amount of radioactive waste is another concern for the replacement in terms of its volume and various types of it that should be categorized before disposal. The regulatory body, NSSC (Nuclear Safety and Security Commission) released a notice related to the classification of radioactive wastes, and most accessory equipment can be classified into the clearance levels, called self-disposal waste. In this study, the practice of self-disposal of metal radioactive waste is carried out to reduce its volume and downgrade its radioactivity. For metal radioactive waste, which is expected to occupy the most amount, analysis status and legal limitations were performed as follows: First, the disposal plan was established after an investigation of the use history for equipment. Second, those were classified by types of materials, and their surface radio-contamination was measured for checking self-disposable or not. After collecting data, the plan for the self-disposal was written and submitted to the Korea Institute of Nuclear Safety (KINS) for approval.

Honey used as conventional medicine has various pharmacological properties. In the honey and anti-inflammatory effect, Gelam honey and Manuka honey has been reported to exert anti-inflammatory activity. However, the anti-inflammatory effect and potential mechanisms of acacia honey (AH) are not well understood. In this study, we investigated anti-inflammatory activity and mechanism of action of AH in LPS-stimulated RAW264.7 cells. AH attenuated NO production through inhibition of iNOS expression in LPS-stimulated RAW264.7 cells. AH also decreased the expressions of IL-1β, IL-6 and TNF-α as pro-inflammatory cytokines, and MCP-1 expression as a pro-inflammatory chemokine. In the elucidation of the molecular mechanisms, AH decreased LPS-mediated IκB-α degradation and subsequent nuclear accumulation of p65, which resulted in the inhibition of NF-κB activation in RAW264.7 cells. AH dose-dependently suppressed LPS-mediated phosphorylation of ERK1/2 and p38 in RAW264.7 cells. In addition, AH significantly inhibited ATF2 phosphorylation and nuclear accumulation of ATF2 in LPS-stimulated RAW264.7 cells. These results suggest that AH has an anti-inflammatory effect, inhibiting the production of pro-inflammatory mediators such as NO, iNOS, TNF-α, IL-6, IL-1β and MCP-1 via interruption of the NF-κB and MAPK/ATF2 signaling pathways.

This study was conducted to investigate the effect of branch extracts of Vaccinium oldhamii (VOB) on melanin synthesis in B16F10 cells. VOB promoted melanin production in absence or presence of α-melanocyte-stimulating hormone (α-MSH) in B16F10 cells. However, VOB did not affect the expression of tyrosinase and TRP-1 associated with melanin synthesis at the mRNA and protein levels in B16F10. But, VOB decreased TRP-2 protein level and induced tyrosinase activation in B16F10 cells. Inhibition of tyrosinase activity and tyrosinase knockdown attenuated VOB-mediated melanin synthesis. In conclusion, VOB may stimulate melanin synthesis through activating tyrosinase activity.

Background : Although the inhibitory effect of mistletoe on cancer cell growth has been reported, the underlying mechanisms to explain its anti-proliferative activity are not fully studied. Thus, we elucidated the potential molecular mechanism of the branch from taxillus yadoriki (TY) parasitic to Neolitsea sericea (NS) (TY-NS-B) for the anti-proliferative effect. Methods and Results : In comparison of anti-proliferative effect of TY from the host trees such as Cryptomeria japonica (CJ), Neolitsea sericea (NS), Prunus serrulata (PS), Cinnamomum camphora (CC) and Quercus acutissima (QA), TY-NS showed higher anti-cell proliferative effect than TY-CJ, TY-PS, TY-CC or TY-QA. In addition, the anti-proliferative effect of branch from TY from all host trees was better than leaves. Thus, we selected the branch from Taxillus yadoriki parasitic to Neolitsea sericea (TY-NS-B) for the further study. TY-NS-B inhibited the cell proliferation in the various cancer cells and downregulated cyclin D1 protein level. MG132 treatment attenuated cyclin D1 downregulation of cyclin D1 protein level by TY-NS-B. In addition, TY-NS-B increased threonine-286 (T286) phosphorylation of cyclin D1, and the mutation of T286 to alanine (T286A) blocked cyclin D1 proteasomal degradation by TY-NS-B. But the upstream factors related to cyclin D1 degradation such as ERK1/2, p38, JNK, GSK3β, PI3K, IκK or ROS did not affect cyclin D1 degradation by TY-NS-B. However, LMB treatment was observed to inhibit cyclin D1 degradation by TY-NS-B, and T286A blocked cyclin D1 degradation through suppressing cyclin D1 redistribution from nucleus to cytoplasm by TY-NS-B. In addition, TY-NS-B activated CRM1 expression. Conclusion : Our results suggest that TY-NS-B may suppress cell proliferation by downregulating cyclin D1 protein level through proteasomal degradation via T286 phosphorylation-dependent cyclin D1 nuclear export. These findings will provide the evidence that TY-NS-B has potential to be a candidate for the development of chemoprevention or therapeutic agents for human cancer.

Background : Vaccinium oldhamii is a Korean native tree, which is deciduous and shrub tree with broad leaf. It was used primarily for edible or medicinal purposes for bladder infection in Korea and China. In addition, it has been reported to be used for treating inflammation, gonorrhea, vomiting, diarrhea and eruption. In this study, we evaluated the anti-inflammatory effect of the branch of Vaccinium oldhamii and elucidated the potential mechanisms in LPS-stimulated RAW264.7 cells. Methods and Results : In the comparative experiment for the inhibitory effect of the plant parts from Vaccinium oldhamii such as fruits, leaves and branches on NO production, we observed that the branch extracts showed the highest inhibitory effect. Thus, the further study was performed using the branch of Vaccinium oldhamii (VOB). VOB did not affect iNOS expression but significantly IL-1β expression, which indicates that VOB may block NO production through the inhibition of IL-1β expression. In elucidation of the potential mechanisms for anti-inflammatory effect, VOB inhibited the degradation of IκB-α which results in the inhibition of p65 nuclear accumulation and NF-κB activation. In addition, VOB suppressed the activation of ERK1/2, p38 and JNK. Conclusion : These results indicate that VOB may exert anti-inflammatory activity through the inhibiting NF-κB and MAPK signaling. From these findings, VOB has potential to be a candidate for the development of chemoprevention or therapeutic agents for the inflammatory diseases.

Background : Hibiscus syriacus is a widely cultivated ornamental shrub, found throughout eastern and southern Asia. The root of H. syriacus has been used in Asian folk medicine as a fungicide, antipyretic, and anthelmintic in the treatment of dysentery, eczema, tinea, and scabies. In this study, we evaluated the anti-inflammatory effect of 70% ethanol extracts of root from Hibiscus syriacus (RHS-E70) and elucidated the potential mechanisms in LPS-stimulated RAW264.7 cells. Methods and Results : RHS-E70 dose-dependently suppressed nitric oxide (NO) production in LPS-stimulated RAW264.7 cells. In addition, RHS-E70 attenuated LPS-mediated overexpression of iNOS and IL-1β. In elucidation of the potential mechanisms for anti-inflammatory effect, RHS-E70 inhibited the phosphorylation and subsequent degradation of IκB-α, which results in the inhibition of p65 nuclear accumulation and NF-κB activation. In addition, RHS-E70 suppressed the activation of ERK1/2 and p38, which results in the inhibition of ATF2 phosphorylation and subsequent ATF2 nuclear accumulation. Conclusion : These results indicate that RHS-E70 may exert anti-inflammatory activity through the inhibiting NF-κB and MAPK signaling. From these findings, RHS-E70 has potential to be a candidate for the development of chemoprevention or therapeutic agents for the inflammatory diseases.

Background : Ginseng (Panax ginseng) has been reported to exert an anti-inflammatory activity in a variety of inflammatory. However, inflammation-regulatory activity of wood-cultivated ginseng has not been thoroughly evaluated. In this study, we evaluated the anti-inflammatory effect of wood-cultivated ginseng and elucidated the potential mechanisms in LPS-stimulated RAW264.7 cells. Methods and Results : Inhibitory effects of the old wood-cultivated ginseng (WCG-O), young wood-cultivated ginseng (WCG-Y) and ginseng (G) on NO and PGE2 production were examined using the Griess assay and ELISA kit. Suppressive effects of WCG-O on inflammatory gene expression, transcriptional activation, and inflammation signaling events were investigated using Western blot analysis, RT-PCR analysis and luciferase activity reporter gene assay. WCG-O dose-dependently suppressed nitric oxide (NO) and Prostaglandin E2 (PGE2) production in LPS-stimulated RAW264.7 cells. In addition, WCG-O attenuated LPS-mediated overexpression of iNOS and COX-2. In addition, WCG-O blocked the expression of TNF-α and IL-1β in LPS-stimulated RAW264.7 cells. In elucidation of the potential mechanisms for anti-inflammatory effect, WCG-O inhibited the activation of IκK-α/β, the phosphorylation of IκB-α, and degradation of IκB-α, which results in the inhibition of p65 nuclear accumulation and NF-κB activation. In addition, WCG-O suppressed the activation of ERK1/2, p38 and JNK, which results in the inhibition of ATF2 nuclear accumulation. Conclusion : These results indicate that WCG-O may exert anti-inflammatory activity through the inhibiting NF-κB and MAPK signaling. From these findings, WCG-O has potential to be a candidate for the development of chemoprevention or therapeutic agents for the inflammatory diseases.

Background : Mistletoe has been used as the herbal medicine to treat hypertension, diabetes mellitus, inflammation, arthritis and viral infection. In this study, we evaluated the anti-inflammatory effect of extracts of branch from Taxillus yadoriki being parasitic in Neolitsea sericea (TY-NS-B) using in vitro model. Methods and Results : TY-NS-B significantly inhibited LPS-induced secretion of NO and PGE2 in RAW264.7 cells. TY-NS-B was also observed to inhibit LPS-mediated iNOS COX-2 expression. In addition, TY-NS-B attenuated production of inflammatory cytokines such as TNF-α and IL-1β induced by LPS. TY-NS-B blocked LPS-mediated inhibitor of IκB-α, and inhibited p65 translocation to the nucleus and NF-κB activation. Furthermore, TY-NS-B reduced the phosphorylation of MAPKs such as p38 and JNK, but not ERK1/2. In addition, TY-NS-B increased ATF3 expression and ATF3 knockdown by ATF3 siRNA attenuated TY-NS-B-mediated inhibition of pro-inflammatory mediator expression. Conclusion : Collectively, our results suggest that TY-NS-B exerts potential anti-inflammatory effects by suppressing NF-κB and MAPK signaling activation, and increasing ATF3 expression. These findings indicate that TY-NS-B could be further developed as an anti-inflammatory drug.

In this study, we elucidated the molecular mechanism of silymarin by which silymarin may inhibits cell proliferation in human colorectal cancer cells in order to search the new potential anti-cancer target associated with the cell growth arrest. Silymarin reduced the level of c-Myc protein but not mRNA level indicating that silymarin-mediated downregulation of c-Myc may result from the proteasomal degradation. In the confirmation of silymarin-mediated c-Myc degradation, MG132 as a proteasome inhibitor attenuated c-Myc degradation by silymarin. In addition, silymarin phosphorylated the threonine-58 (Thr58) of c-Myc and the point mutation of Thr58 to alanine blocked its degradation by silymarin, which indicates that Thr58 phosphorylation may be an important modification for silymarin-mediated c-Myc degradation. We observed that the inhibition of ERK1/2, p38 and GSK3β blocked the Thr58 phosphorylation and subsequent c-Myc degradation by silymarin. Finally, the point mutation of Thr58 to alanine attenuated silymarin-mediated inhibition of the cell growth. The results suggest that silymarin induces the cell growth arrest through c-Myc proteasomal degradation via ERK1/2, p38 and GSK3β-dependent Thr58 phosphorylation.