Parameters optimization using an artificial neural networks and release characteristics of humic acids during lignite bioconversion.

The bioconversion of coal at ambient conditions is a promising technology for coal processing. However, there are few examples of the optimization of processes for industrial-scale use. In this work, the optimization of process parameters affecting lignite bioconversion by an isolated fungus WF8 using an artificial neural network (ANN) combined with a genetic algorithm (GA) was carried out for modeling of humic acids (HAs) yield and parameters. Kinetic models were used to understand the release characteristics of HAs from the bioconversion of lignite. The results of the present work indicate that the optimal process parameters (OPP) are 29 °C, initial pH of 7, 180 rpm, 0.6 mmol·L-1 of CuSO4, 0.4 mmol L-1 of MnSO4, and 6.4 µmol·L-1 of veratryl alcohol (VA). The predicted experimental data obtained by ANN is similar to the actual and the significant correlation coefficient value (R2) of 0.99 indicates that ANN has good predictability. The actual yield of HAs are 5.17 mg·mL-1. During bioconversion, the fungus WF8 could loosen and attack the structure of lignite. The release of HAs produced by bioconversion of lignite under the OPP via diffusion and swelling is fit to zero-order model independent on concentration. This provides support for the industrial bioconversion of lignite.

Aldehyde dehydrogenase 2 protects against sympathetic excitation-induced cardiac fibrosis.

Sympathetic stimulated-cardiac fibrosis imposes great significance on both disease progression and survival in the pathogenesis of many cardiovascular diseases. However, there are few effective therapies targeting it clinically. The cardioprotective effect of aldehyde dehydrogenase 2 (ALDH2) has been explored in many pathological conditions, whether it can exert benefit effects on chronic sympathetic stimulus-induced cardiac fibrosis remains unclear. In this study, we determined to explore the role of ALDH2 on isoproterenol (ISO)-induced cardiac fibroblasts (CF) proliferation and cardiac fibrosis. It was found that ALDH2 enzymatic activity was impaired in ISO-induced HCF proliferation and Aldh2 deficiency promoted mouse CF proliferation. Alda-1, an ALDH2 activator, exerted obvious suppressive effect on ISO-induced HCF proliferation, together with the induction of cell cycle arrest at G0/G1 phase and decreased expression of cyclin E1 and cyclin-dependent kinase 2 (CDK2). Mechanistically, the inhibitory role of Alda-1 on HCF proliferation was achieved by decreasing mitochondrial reactive oxygen species (ROS) production, which was partially reversed by rotenone, an inducer of ROS. In addition, wild-type mice treated with Alda-1 manifested with reduced fibrosis and better cardiac function after ISO pump. In summary, Alda-1 alleviates sympathetic excitation-induced cardiac fibrosis via decreasing mitochondrial ROS accumulation, highlighting ALDH2 activity as a promising drug target of cardiac fibrosis.

Late cardioprotection of exercise preconditioning against exhaustive exercise-induced myocardial injury by up-regulatation of connexin 43 expression in rat hearts.

OBJECTIVE: To investigate the expression of myocardium connexin 43 (Cx43) in late exercise preconditioning (LEP) cardioprotection. METHODS: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups (n = 8). Myocardial injury was judged in accordance with serum levels of cTnⅠ and NT-proBNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 mRNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting. RESULTS: The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 mRNA level between the four groups. Cx43 protein level was decreased significantly in group EE (P < 0.05). However, LEP produced a significant increase in Cx43 protein level (P < 0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP (P < 0.05). CONCLUSIONS: LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.