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  • Author or Editor: Z. Song x
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Abstract  

The heat capacities of fenpropathrin in the temperature range from 80 to 400 K were measured with a precise automatic adiabatic calorimeter. The fenpropathrin sample was prepared with the purity of 0.9916 mole fraction. A solid—liquid fusion phase transition was observed in the experimental temperature range. The melting point, T m, enthalpy and entropy of fusion, fus H m, fus S m, were determined to be 322.48±0.01 K, 18.57±0.29 kJ mol–1 and 57.59±1.01 J mol–1 K–1, respectively. The thermodynamic functions of fenpropathrin, H (T)H (298.15), S (T)S (298.15) and G (T)G (298.15), were reported with a temperature interval of 5 K. The TG analysis under the heating rate of 10 K min–1 confirmed that the thermal decomposition of the sample starts at ca. 450 K and terminates at ca. 575 K. The maximum decomposition rate was obtained at 558 K. The purity of the sample was determined by a fractional melting method.

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Abstract

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 (E a) 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 C p mode of microcalorimeter. Using the relationship between C p 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.

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Abstract

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.

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