Chenyang Qi

Monitoring radioactivity levels in the environment around nuclear power plants is of great significance to assessing environmental safety and impact. Shidaowan nuclear power plant is currently undergoing commissioning; however, the baseline soil radioactivity is unknown. The naturally occurring radionuclides ²³⁸U, ²³²Th, ²²⁶Ra and ⁴⁰K, and artificial radionuclide (AR) ¹³⁷Cs in soil samples around the Shidaowan nuclear power plant were measured to establish the baseline levels. Human health hazard indices such as external hazard indices (H_ex), Radium equivalent (Ra_eq), outdoor absorbed dose rate (D_out), annual effective dose (AED) and excess lifetime cancer risk (ELCR) were estimated. The average concentration of ²³²Th, ⁴⁰K, ¹³⁷Cs, ²³⁸U and ²²⁶Ra were 42.6 ± 15, 581 ± 131, 0.68 ± 0.38, 40.13 ± 9.07 and 40.8 ± 12.8 Bq per kg, respectively. The average H_ex, Ra_eq, D_out, AED and ELCR were 0.40, 146 Bq per kg, 68.8 nGy per h, 0.09 mSv per y and 3.29E-04, respectively. These data showed an acceptable level of risk to residents near the nuclear power plant and that the current radioactivity in the soil may not pose immediate harm to residents living close to the nuclear power plant. The observed lower AED and 40 K and 137Cs concentrations were comparable to other studies, whilst ELCR was higher than the world average of 2.9E-04. The commissioning of the Shidaowan nuclear power plant is potentially safe for the surrounding residents; further continuous monitoring is recommended.

Cell cycle checkpoint kinases play a pivotal role in protecting against replicative stress. In this study, valproic acid (VPA), a histone deacetylase inhibitor (HDACi), was found to promote breast cancer MCF-7 cells to traverse into G2/M phase for catastrophic injury by promoting PPP2R2A (the B-regulatory subunit of Phosphatase PP2A) to facilitate the dephosphorylation of Chk1 at Ser317 and Ser345. By contrast, VPA protected normal 16HBE cells from HU toxicity through decreasing PPP2R2A expression and increasing Chk1 phosphorylation. The effect of VPA on PPP2R2A was at the post-transcription level through HDAC1/2. The in vitro results were affirmed in vivo. Patients with lower PPP2R2A expression and higher pChk1 expression showed significantly worse survival. PPP2R2A D197 and N181 are essential for PPP2R2A-Chk1 signaling and VPA-mediated bidirectional effect on augmenting HU-induced tumor cell death and protecting normal cells.