Influence Mechanism of Initial Concreting Temperature and Water-Binder Ratio on Hydration Rate of Fly Ash Concrete.

The hydration exothermic rate of fly ash concrete is significantly affected by the initial concreting temperature and water-binder ratio. Firstly, the adiabatic temperature rise and temperature rise rate of fly ash concrete at different initial concreting temperatures and water-binder ratios were obtained by a thermal test instrument; then, the effects of initial concreting temperature and water-binder ratio on the hydration kinetic parameters of the NG-I-D hydration process of fly ash concrete were analyzed by the theory of hydration kinetics; lastly, the effects of initial concreting temperature and water-binder ratio on chemically bound water and pore bulk of fly ash concrete during hydration were analyzed by applying a thermogravimetric analyzer and industrial CT scanning techniques. The results showed that the increase in initial concreting temperature and the decrease in water-binder ratio accelerated the rate of temperature rise, and the initial concreting temperature had a more significant effect than the water-binder ratio. During the hydration reaction, the I process was significantly influenced by the initial concreting temperature, and the D process was significantly influenced by the water-binder ratio; the content of bound water increased with the increase in water-binder ratio and age and the decrease in initial concreting temperature. The initial temperature had a significant effect on the growth rate of 1 to 3 days bound water, and the water-binder ratio had a more significant effect on the growth rate of 3 to 7 days bound water. The porosity was positively correlated with the initial concreting temperature and water-binder ratio and decreased with age, but 1 to 3 days was the key period of porosity change. Additionally, the pore size was also influenced by the initial concreting temperature and water-binder ratio.

Mycobacterium tuberculosis Rv0927c Inhibits NF-κB Pathway by Downregulating the Phosphorylation Level of IκBα and Enhances Mycobacterial Survival.

Through long-term coevolution with its host, Mycobacterium tuberculosis (M. tuberculosis) uses multiple strategies to escape host defenses. The M. tuberculosis Rv0927c protein is predicted to be a short-chain dehydrogenase/reductase related to bacterial metabolism. However, the role of Rv0927c during M. tuberculosis infection remains unclear. Here, we observed that Rv0927c inhibited the expression of IL-6, TNF-α, and IL-1ß, an effect dependent on NF-κB and p38 pathways. Western blot analysis of macrophages infected with recombinant Mycobacterium smegmatis strains showed that Rv0927c attenuated NF-κB activation by downregulating the phosphorylation of IκBα. Additionally, Rv0927c enhanced intracellular survival of M. smegmatis and pathological effects in mice. In conclusion, our findings demonstrate that Rv0927c functions as a regulator of inflammatory genes and enhances the survival of M. smegmatis.