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Sarin (GB) and soman (GD) are severely toxic nerve agents that react slowly in water, resulting in long-term poisoning of the water and a serious threat to personnel. Some ions can catalyse GB and GD hydrolysis in water; the relevant research for GB is detailed, whereas that for GD is relatively less so. In this paper, GD hydrolysis catalysed by hypochlorite (ClO−) ions was studied via kinetic experiments. A fluorite-ion-specific electrode was used to monitor F− ions produced, allowing the rate constant and half-life of the GD hydrolysis to be calculated. The results showed that ClO− ions promote GD hydrolysis well; the higher the concentration of ClO−, the faster the GD was hydrolysed. In NaClO solution at pH 8.0 with 3.22×10–3 M ClO− ions, the half-life of GD hydrolysis was 82.5 s, about 875 times shorter than that in water at pH 8.0. The rate constant for catalysis of GD hydrolysis by ClO- ions ++(kc1o−)++ was 2.6 M−1 s−1, about one quarter the value of ++koh− ++but over 1500 times greater than kB and ++kPO4,++ with B representing N-2-hydroxyethylpiperazine-N’-2-ethanesulfonic acid present as a free base; this result indicated that ClO− ions catalyse GD hydrolysis well.

Iron overload can lead to chronic complications, serious organ dysfunction or death in the body. Under hypoxic conditions, the body needs more iron to produce red blood cells to adapt to the hypoxic environment. The prevalence of iron overload in the Tibetan population is higher than that in the Han population. To explore the molecular mechanism of iron-overload in the Tibetan population, this study investigated the transcriptome of the Tibetan iron overload population to obtain differentially expressed genes (DEGs) between the iron-overloaded population and the normal iron population. Functional enrichment analysis identified key related pathways, gene modules and coexpression networks under iron-overload conditions, and the 4 genes screened out have the potential to become target genes for studying the development of iron overload. A total of 28 pathways were screened to be closely related to the occurrence and development of iron overload, showing that iron overload is extremely related to erythrocyte homeostasis, cell cycle, oxidative phosphorylation, immunity, and transcriptional repression.