[en] Highlights: • TGEV N protein reduces cell viability by inducing cell cycle arrest and apoptosis. • TGEV N protein induces cell cycle arrest and apoptosis by regulating p53 signaling. • TGEV N protein plays important roles in TGEV-induced cell cycle arrest and apoptosis. - Abstract: Our previous studies showed that TGEV infection could induce cell cycle arrest and apoptosis via activation of p53 signaling in cultured host cells. However, it is unclear which viral gene causes these effects. In this study, we investigated the effects of TGEV nucleocapsid (N) protein on PK-15 cells. We found that TGEV N protein suppressed cell proliferation by causing cell cycle arrest at the S and G2/M phases and apoptosis. Characterization of various cellular proteins that are involved in regulating cell cycle progression demonstrated that the expression of N gene resulted in an accumulation of p53 and p21, which suppressed cyclin B1, cdc2 and cdk2 expression. Moreover, the expression of TGEV N gene promoted translocation of Bax to mitochondria, which in turn caused the release of cytochrome c, followed by activation of caspase-3, resulting in cell apoptosis in the transfected PK-15 cells following cell cycle arrest. Further studies showed that p53 inhibitor attenuated TGEV N protein induced cell cycle arrest at S and G2/M phases and apoptosis through reversing the expression changes of cdc2, cdk2 and cyclin B1 and the translocation changes of Bax and cytochrome c induced by TGEV N protein. Taken together, these results demonstrated that TGEV N protein might play an important role in TGEV infection-induced p53 activation and cell cycle arrest at the S and G2/M phases and apoptosis occurrence

[en] Highlights: • SAC radwaste matrix have the low leaching rate and cumulative leaching fraction. • The leaching mechanism and model of Cs⁺ and Sr²⁺ were clarified. • Sr²⁺ and Cs⁺ could enter negative channel of ettringite, Sr²⁺ also replace its Ca²⁺ • The absorption mechanism of AHG for nuclides was found. Radioactive ion exchange resin is a problematic waste requiring proper immobilization to ensure that the resin's radioactive ions are stable for storage and ultimate disposal in water environments, such as seawater or groundwater. Sulphoaluminate cement hardened paste, with the dense structure, great retention capacity for ions, and resistance to SO₄²⁻ and Cl⁻, is a potential cementation material to encapsulate ¹³⁷Cs⁺ and ⁹⁰Sr²⁺ in radioactive ion exchange resin. The leaching rates of Cs⁺ and Sr²⁺ from the sulfoaluminate cement matrix solidifying radioactive ion exchange resin and their immobilization characteristics of the predominant hydration products (ettringite; aluminum hydroxide gel) of sulfoaluminate cement were investigated in depth. The experimental results showed that the sulphoaluminate cement radwaste matrix had a better retention capacity for Cs⁺ and Sr²⁺ than the OPC radwaste matrix. The 42 days cumulative leaching fractions of Cs⁺ and Sr²⁺ were 6.21 × 10⁻² and 5.77 × 10⁻³ cm, respectively, which could be described by the FRDM or DDIM model for Cs⁺, and the DDIM model for Sr²⁺. The retention of Cs⁺ and Sr²⁺ originated from the chemical absorption by ettringite, aluminum hydroxide gel, and the physical barrier. The ettringite and aluminum hydroxide gel's retention rates for Cs⁺ are above 70% and 40%, respectively, while those of Sr²⁺ are above 88% and 10%, respectively. In detail, Cs⁺ and Sr²⁺ could be absorbed by both ettringite and aluminum hydroxide gel. Unlike Cs⁺, Sr²⁺ could enter the ettringite's crystal lattice by replacing Ca²⁺ and entering the negative channel.