Selective Adsorption of Sr(II) from Aqueous Solution by Na3FePO4CO3: Experimental and DFT Studies.

The efficient segregation of radioactive nuclides from low-level radioactive liquid waste (LLRW) is paramount for nuclear emergency protocols and waste minimization. Here, we synthesized Na3FePO4CO3 (NFPC) via a one-pot hydrothermal method and applied it for the first time to the selective separation of Sr2+ from simulated LLRW. Static adsorption experimental results indicated that the distribution coefficient Kd remained above 5000 mL·g-1, even when the concentration of interfering ions was more than 40 times that of Sr2+. Furthermore, the removal efficiency of Sr2+ showed no significant change within the pH range of 4 to 9. The adsorption of Sr2+ fitted the pseudo-second-order kinetic model and the Langmuir isotherm model, with an equilibrium time of 36 min and a maximum adsorption capacity of 99.6 mg·g-1. Notably, the adsorption capacity was observed to increment marginally with an elevation in temperature. Characterization analyses and density functional theory (DFT) calculations elucidated the adsorption mechanism, demonstrating that Sr2+ initially engaged in an ion exchange reaction with Na+. Subsequently, Sr2+ coordinated with four oxygen atoms on the NFPC (100) facet, establishing a robust Sr-O bond via orbital hybridization.

Study on the migration performance of Cs(I) in the treatment of simulated radioactive wastewater by electrodialysis.

As a competitive radioactive wastewater treatment technology, electrodialysis (ED) has the advantages of low operating pressure and high cycles of concentration. In order to analyze the migration performance of radionuclides during the treatment of radioactive wastewater by ED, a radionuclide migration model was constructed based on the mass conservation law and Faraday's law with the typical radionuclide cesium as the research object. Experiments were carried out for the treatment of simulated radioactive wastewater in a small-scale ED system, and the average migration rate of radionuclides under different operating conditions was predicted by the model. The results showed that the experimental values of concentration and average migration rate of Cs(I) were significantly correlated with the calculated values of the model, in which the relative error of the average migration rate was 4.54%. The variation characteristics of Cs(I) concentration in diluted solution under different current and volume ratio conditions can be predicted by the model. The average variation rate of Cs(I) concentration decreases significantly with the increase of current and volume ratio.

LATS2 promotes apoptosis in non-small cell lung cancer A549 cells via triggering Mff-dependent mitochondrial fission and activating the JNK signaling pathway.

LATS2 is a classical tumor suppressor that affects non-small cell lung cancer proliferation and mobilization. However, its role in lung cancer cell apoptosis is unknown. The aim of our study is to explore whether LATS2 activates mitochondria-related apoptosis in lung cancer cells. In the present study, A549 non-small cell lung cancer cells were transfected with a LATS2 adenovirus to induce LATS2 overexpression. Cell apoptosis was evaluated via the MTT assay, TUNEL staining, western blotting, trypan blue staining and ELISA. Mitochondrial function was measured using an immunofluorescence assay, western blotting and ELISA. The results demonstrated that LATS2 was downregulated in A549 lung cancer cells. Overexpression of LATS2 induced A549 cell apoptosis via activating mitochondrial fission. Subsequently, we confirmed that LATS2 modulated mitochondrial fission via the JNK-Mff signaling pathway. Inhibition of the JNK pathway and/or knockdown of Mff abolished the pro-apoptotic effect of LATS2 on A549 cells. Taken together, our results identified LATS2 as a classical tumor suppressor of lung cancer via triggering mitochondrial fission and activating the JNK-Mff signaling pathway. Our results lay the foundation for detailed study of the molecular mechanisms of LATS2 overexpression and regulation of mitochondrial fission for lung cancer treatment.