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The Study on the Way of Radioactive Waste Disposal in China
Keyan Teng,Hao Peng,Caixia Lv,Han Wu 한국방사성폐기물학회 2022 방사성폐기물학회지 Vol.20 No.4
Because of the massive development of nuclear power plants in China in recent years, China is facing the challenge of radioactive waste disposal. China has established complete regulatory requirements for radioactive waste disposal, but it also has encountered problems and challenges in low-level radioactive waste disposal in terms of management, selection of disposal facility sites, and implementation of a site selection plan. Three low-level radioactive waste disposal facilities that have been operated in China are described, and their activity limits, locations, and capacities are also outlined. The connotations of “regional” and “centralized” disposal policies are discussed in light of the characteristics of the radioactive waste. The characteristics and advantages of the regional and centralized disposal policies are compared. It is concluded that the regional disposal policy adopted in 1992 can no longer meet the current disposal needs, and China should adopt a combination of the two disposal policies to solve the problem of radioactive waste disposal.
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Epigenetic silencing of UBXN8 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
Yang Erna,Guan Wei,Gong Desheng,Li Jieying,Han Caixia,Zhang Juan,Wang Hong,Kang Synat,Gao Xuefeng,Li Yonghui,Yu Li 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1- RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1+ AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1+ cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1- RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML. The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1-RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1 + AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1 + cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1-RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML.
ScienceON
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