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In the process of electrokinetic (EK) remediation of uranium-contaminated soil, the existence form of uranium in soil pore fluid will affect on its migration behavior. In this paper, a novel type of electrolyte (citric acid + ferric chloride, CA+ FeCl 3 ) has been investigated for the EK remediation of uranium-contaminated red soil. The effects of different electrolyte and the concentrations of FeCl 3 on migration behavior of U(VI) and environmental risks were investigated after EK remediation. The result showed that the optimum concentration was 0.1 mol/L CA mixed with 0.03 mol/L FeCl 3 in this study. At this time, the removal efficiency of uranium was about 61.55 ± 0.41%, and the cumulative energy consumption was 0.2559 kWh. Compared with deionized water and single CA, combined CA with FeCl 3 has the advantages of high removal efficiency, low leaching toxicity, and less damage to the soil after the electrokinetic remediation treatment.

The purpose of this study is to test the hypothesis that the mammalian target of rapamycin (mTOR) signaling pathway might mediate neuroprotection in a mouse model of septic encephalopathy and also to identify the role of autophagy. Mice were subjected to cecal ligation and puncture (CLP) or a sham operation, and all 50 mice were randomly assigned to five groups: sham, CLP+ saline, CLP+ rapamycin (1, 5, 10 mg/kg) groups. Two weeks after the operation, Morris water maze was conducted for behavioral test; Nissl staining was used for observing glia infiltration; immunohistochemical staining and biochemical measures in hippocampi were performed to detect mTOR targets and autophagy indicators. Immunochemistry revealed significant loss of neurons and increased glia infiltration in hippocampus after CLP operation. Inhibition of mTOR by rapamycin rescued cognitive deficits caused by sepsis (p < 0.05). Rapamycin did not affect total mTOR targets, while phosphorylated mTOR targets (p-mTOR-Ser2448, p-p70S6k-Thr389, p-AKT-S473) decreased (p < 0.05) and autophagy indicators (LC3-II, Atg5, Atg7) were increased, and P62 was decreased in rapamycin-treated CLP mice compared with the untreated (p < 0.05) in hippocampus. Rapamycin improves learning after sepsis through enhancing autophagy and may be a potentially effective therapeutic agent for the treatment of sepsis-induced cognitive impairment.

Over-expression of P-glycoprotein (Pgp), a protein responsible for multidrug resistance (MDR), is responsible for general resistance to anti-epileptic drugs (AEDs). We explored the potential use of gene therapy with adenoviral-delivered RNA interference against mdr1b as a method to sensitize refractory epilepsy to AEDs. We constructed replication-deficient recombinant adenovirus Adeno-mdr1b1 carrying short hairpin RNA (shRNA) targeting against mdr1b, and successfully infected the established Sprague-Dawley rat astrocyte model of Coriaria Lactone-induced Pgp over-expression. The expression levels of mdr1b and Pgp and the Rhodamine123 efflux ratio in trial groups were significantly lower than that of blank control (P < 0.05) during the first 7 days post-infection, with the most inhibition at 48 h. The results suggest that knockdown of MDR using adenovirus not only avoided the toxicity and low rate of plasmid nucleofection, but also overcame its poor efficiency of mdr1b silencing. More importantly, this study may pave the way for a promising approach to remedy refractory epilepsy.