Authors:L. Yang, Li Sun, Fen Xu, J. Zhang, J. Zhao, Z. Zhao, C. Song, R. Wu, and Riko Ozao
The microcalorimetric method has been used to study the effects of cefpiramide and ceftizoxime sodium on the E. coli growth. The results revealed that these two cephalosporins may alter the metabolic way of the E. coli. Moreover, the lethal doses of cefpiramide and ceftizoxime sodium are 2.000 and 0.2000 μg mL−1, respectively. Combining with the relationships between growth rate constant (k), the maximum power output (Pm), the time corresponding to the maximum power output (tm) and cephalosporins concentration (C), one can draw the conclusion that the ceftizoxime sodium has a stronger inhibition effects on the growth of E. coli than that of cefpiramide and they both have the possibility to induce the drug fever.
Authors:H. X. Ma, B. Yan, Y. H. Ren, Y. Hu, Y. L. Guan, F. Q. Zhao, J. R. Song, and R. Z. Hu
3,3-Dinitroazetidinium (DNAZ) salt of perchloric acid (DNAZ·HClO4) was prepared, it was characterized by the elemental analysis, IR, NMR, and a X-ray diffractometer. The thermal behavior and decomposition reaction kinetics of DNAZ·HClO4 were investigated under a non-isothermal condition by DSC and TG/DTG techniques. The results show that the thermal decomposition process of DNAZ·HClO4 has two mass loss stages. The kinetic model function in differential form, the value of apparent activation energy (Ea) and pre-exponential factor (A) of the exothermic decomposition reaction of DNAZ·HClO4 are f(α) = (1 − α)−1/2, 156.47 kJ mol−1, and 1015.12 s−1, respectively. The critical temperature of thermal explosion is 188.5 °C. The values of ΔS≠, ΔH≠, and ΔG≠of this reaction are 42.26 J mol−1 K−1, 154.44 kJ mol−1, and 135.42 kJ mol−1, respectively. The specific heat capacity of DNAZ·HClO4 was determined with a continuous Cp mode of microcalorimeter. Using the relationship between Cp and T and the thermal decomposition parameters, the time of the thermal decomposition from initiation to thermal explosion (adiabatic time-to-explosion) was evaluated as 14.2 s.
Authors:Z.K. Xie, S.Y. Yu, M. He, S.X. Yu, H.F. Xiao, and Y.D. Song
In this paper, we studied the inhibitory effect of oleanolic acid (OA) on non-enzymatic glycosylation and the improvement of glycometabolism in insulin resistant (IR) human liver tumour (HepG2) cells. The anti-glycosylation activity of OA was determined by bovine serum albumin (BSA) fructose model. The results showed that OA moderately inhibited the formation of the intermediates of non-enzymatic glycosylation, fructosamine and α-dicarbonyl compounds, and strongly inhibited the formation of advanced glycation end products (AGEs). In addition, we analysed the effect of OA on glycometabolism induced by palmitic acid (PA) in HepG2 cells. The results showed that OA had almost no impact on HepG2 cell viability at concentrations lower than 30 µM. With the increase of OA concentration, glucose production in IR HepG2 cells decreased, while glycogen content increased. Meanwhile, OA has a significant inhibitory effect on reactive oxygen species (ROS) levels in IR-HepG2 cells. Those results suggested that OA could be a promising natural blood glucose decreasing substance in the pharmaceutical and functional food industries.