• Proceedings of the Korean Nuclear Society Conference
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• 2005.10a
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• pp.1021-1022
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• 2005

• Proceedings of the Korea Society for Energy Engineering kosee Conference
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• 2002.05a
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• pp.135-141
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• 2002

An optimization of KTF thorium fuel assembly design was performed on the basis of the design parameter studies. Optimization goals ware to make the core have both proliferation resistance and fuel cycle economics. Four kinds of proliferation resistance indexes were used; SNS, TG, BCM, Toxicity. A new index, FEI was regarded as a limiting index for the maximization of fuel cycle economics. Optimized thorium fuel design was applied for APR-1400 reactor core. Nuclear core design procedures were examined to solve the thorium fuel reactor problems. It was shown that heterogeneous thorium fuel core option is acceptable in safety and economics aspects.

• Journal of Energy Engineering
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• v.20 no.3
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• pp.236-241
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• 2011

In this study, considering a degree of proliferation resistance and sustainability, development status of perspective recycling systems for spent nuclear fuels (SNF) is comprehensively reviewed on the basis of the urgent needs of sustainable management measures for high level radioactive wastes such as spent nuclear fuels (SNF).

• Archives of Pharmacal Research
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• v.22 no.1
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• pp.1-8
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• 1999

Transforming growth factor-$\beta$ (TGF-$\beta$) is the prototypical multifunctional cytokine, participating in the regulation of vital cellular activities such as proliferation and differentiations as well as a number of basic physiological functions. The effects of TGF-$\beta$ are critically dependent on the expression and distribution of a family of TGF-$\beta$ receptors, the TGF-$\beta$ types I, II, and III. It is now known that a wide variety of human pathology can be caused by aberrant expression and function of these receptors. the coding sequence of the type II receptor (RII) appears to render it uniquely susceptible to DNA replication errors in the course of normal cell division. By virtue of its key role in the regulation of cell proliferation, TGF-$\beta$ RII should be considered as a tumor suppressor gene. High levels of mutation in the TGF-$\beta$ RII gene have been observed in a wide range of primarily epithelial malignancies, including colon and gastric cancer. It appears likely that mutation of the TGF-$\beta$ RII gene may be a very critical step in the pathway of carcinogenesis.

• BMB Reports
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• v.52 no.5
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• pp.330-335
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• 2019

Hepatitis B virus (HBV) encoding the HBV x protein (HBx) is a known causative agent of hepatocellular carcinoma (HCC). Its pathogenic activities in HCC include interference with several signaling pathways associated with cell proliferation and apoptosis. Mutant C-terminal-truncated HBx isoforms are frequently found in human HCC and have been shown to enhance proliferation and invasiveness leading to HCC malignancy. We investigated the molecular mechanism of the reduced doxorubicin cytotoxicity by C-terminal truncated HBx. Cells transfected with C-terminal truncated HBx exhibited reduced cytotoxicity to doxorubicin compared to those transfected with full-length HBx. The doxorubicin resistance of cells expressing C-terminal truncated HBx correlated with upregulation of the ATP binding cassette subfamily B member 1(ABCB1) transporter, resulting in the enhanced efflux of doxorubicin. Inhibiting the activity of ABCB1 and silencing ABCB1 expression by small interfering ribonucleic acid (siRNA) increased the cytotoxicity of doxorubicin. These results indicate that elevated ABCB1 expression induced by C-terminal truncation of HBx was responsible for doxorubicin resistance in HCC. Hence, co-treatment with an ABCB1 inhibitor and an anticancer agent may be effective for the treatment of patients with liver cancer containing the C-terminal truncated HBx.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.427-432
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• 2014

Isocitrate dehydrogenase (IDH) is of great importance in cell metabolism and energy conversion. IDH mutation in glioma cells is reported to be associated with an increased overall survival. However, effects biological behavior of therapy of gliomas are unclear. Here, we investigated the influence of wild-type and mutated IDH genes on glioma cell biological behavior and response to chemotherapy. Relevant mechanisms were further explored. We designed our study on the background of the IDHR132H mutation. Stable cell lines were constructed by transfection. The CCK-8 method was used to assess cell proliferation, flow cytometry for the cell cycle and cell apoptosis, and the transwell method for cell invasion. Nude mouse models were employed to determine tumorigenesis and sensitivity to chemotherapy. Western blotting was used to detect relevant protein expression levels. We found that overexpression of wild IDH1 gene did not cause changes in the cell cycle, apoptosis and invasion ability. However, it resulted in chemotherapy resistance to a high dose of temozolomide (TMZ) in vivo and in vitro. The IDH1 mutation caused cell cycle arrest in G1 stage and a reduction of proliferation and invasion ability, while raising sensitivity to chemotherapy. This may provide an explanation for the better prognosis of IDH1 mutated glioma patients and the relative worse prognosis of their wild-type IDH1 counterparts. We also expect IDH1 mutations may be optimized as new targets to improve the prognosis of glioma patients.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.7
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• pp.4249-4254
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• 2013

Background: Parafibromin is a protein encoded by the HRPT2 (hyperparathyroidism 2) oncosuppressor gene and its down-regulated expression is involved in pathogenesis of parathyroid, breast, gastric and colorectal carcinomas. This study aimed to clarify the effects of parafibromin expression on the phenotypes and relevant mechanisms of DLD-1 colon carcinoma cells. Methods: DLD-1 cells transfected with a parafibromin-expressing plasmid were subjected to examination of phenotype, including proliferation, differentiation, apoptosis, migration and invasion. Phenotype-related proteins were measured by Western blot. Parafibromin and ki-67 expression was detected by immunohistochemistry on tissue microarrays. Results: The transfectants showed higher proliferation by CCK-8, better differentiation by electron microscopy and ALP activity and more apoptotic resistance to cisplatin by DNA fragmentation than controls. There was no difference in early apoptosis by annexin V, capase-3 activity, migration and invasion between DLD-1 cells and their transfectants. Ectopic parafibromin expression resulted in down-regulated expression of smad4, MEKK, GRP94, GRP78, $GSK3{\beta}$-ser9, and Caspase-9. However, no difference was detectable in caspase-12 and -8 expression. A positive relationship was noted between parafibromin and ki-67 expression in colorectal carcinoma. Conclusions: Parafibromin overexpression could promote cell proliferation, apoptotic resistance, and differentiation of DLD-1 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8067-8073
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• 2016

Background: Long non-coding RNAs (lncRNAs) are emerging as key players in gene expression that govern cell developmental processes, and thus contributing to diseases, especially cancers. Many studies have suggested that aberrant expression of lncRNAs is responsible for drug resistance, a substantial obstacle for cancer therapy. Drug resistance not only results from individual variations in patients, but also from genetic and epigenetic differences in tumors. It is reported that drug resistance is tightly modulated by lncRNAs which change the stability and translation of mRNAs encoding factors involved in cell survival, proliferation, and drug metabolism. In this review, we summarize recent advances in research on lncRNAs associated with drug resistance and underlying molecular or cellular mechanisms, which may contribute helpful approaches for the development of new therapeutic strategies to overcome treatment failure.

• Asia-Pacific Journal of Business
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• v.12 no.4
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• pp.313-329
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• 2021

Purpose - Digital trade, which started in the early 2000s, is showing a sharp increase due to the recent pandemic. However, despite this proliferation, users' acceptance of innovation is very slow. Cloud services are at the center of digital trade activation. This study aims to contribute to the spread of digital trade through empirical analysis of the resistance factors that hinder the use of cloud service-based digital trade using the innovation resistance theory and the status quo bias theory. Design/Methodology/Approach - In order to achieve the research purpose, this study was conducted with 171 entrepreneurs using cloud service-based digital trade. Structural equation model(SEM) was used through empirical analysis. Findings - As a result of the study, it was found that the complexity of technology, perceived risk, compatibility, and trust in service providers had a significant effect on innovation resistance, and policy trust did not affect innovation resistance. Also, security concerns and institutional trust were analyzed to have a significant effect on the trust of service providers. Research Implications - This study is meaningful to help the rapid diffusion of innovative technologies through empirical analysis of factors that lower the intention to accept cloud service-based digital trade.

• Journal of Ginseng Research
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• v.34 no.3
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• pp.192-197
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• 2010

Recent studies have indicated that $\beta$-cell dysfunction and insulin resistance are important factors in the development of type 2 diabetes. The present study investigated the effect of extracts from different parts of white, Taegeuk, and red ginseng root on insulin-stimulated glucose uptake in muscle cells and proliferation of $\beta$-cells. Extracts of the fine roots of Taegeuk ginseng significantly enhanced glucose uptake compared with the control. White ginseng lateral root extracts enhanced insulin-induced glucose uptake. Proliferation of $\beta$-cells was significantly increased by Taegeuk ginseng main and lateral root extracts and by red ginseng lateral and fine root extracts. In conclusion, different root parts of white, Taegeuk, and red ginseng differentially affect glucose uptake and pancreatic $\beta$-cell proliferation.