A first-order kinetic model for simulating the aerobic degradation of municipal solid waste.

Aerobic degradation models are important tools for investigating the aerobic degradation behavior of municipal solid waste (MSW). In this paper, a first-order kinetic model for aerobic degradation of MSW was developed. The model comprehensively considers the aerobic degradation of five substrates, i.e., holocellulose, non-cellulosic sugars, proteins, lipids and lignin. The proportion ranges of the five substrates are summarized with the recommended values given. The effects of temperature, moisture content, oxygen concentration and free air space (FAS) on the reaction rates are considered, and the effect of settlement is accounted for in the FAS correction function. The reliability of the model was verified by comparing simulations of the aerobic degradation of low food waste content (LFWC-) and high food waste content (HFWC-) MSWs to the literature. Afterwards, a sensitivity analysis was carried out to establish the relative importance of aeration rate (AR), volumetric moisture content (VMC), and temperature. VMC had the greatest influence on the aerobic degradation of LFWC-MSW, followed by temperature and then AR; for HFWC-MSW, temperature was the most important factor, then VMC and last was AR. The degradation ratio of LFWC-MSW can reach 98.0% after 100 days degradation under its optimal conditions (i.e., temperature: 55 °C, VMC: 40%, AR: 0.16 L min-1 kg-1 DM), while it is slightly higher as 99.5% for HFWC-MSW under its optimal conditions (i.e., temperature: 55 °C, VMC: 40%, AR: 0.20 L min-1 kg-1 DM).

DHI Increases the Proliferation and Migration of Schwann Cells Through the PI3K/AKT Pathway and the Expression of CXCL12 and GDNF to Promote Facial Nerve Function Repair.

The facial nerve is one of the vulnerable nerves in otolaryngology. Repair and recovery of facial nerve injury have a high priority in clinical practice. The proliferation and migration of Schwann cells are considered of great significance in the process of nerve injury repair. Danhong injection (DHI), as a common drug for cardiovascular and cerebrovascular diseases, has been fully certified in neuroprotection research, but its role in facial nerve injury is still not clear. Our study found that DHI can promote the proliferation and migration of RSC96 cells, a Schwann cell line, and this effect is related to the activation of the PI3K/AKT pathway. LY294002, an inhibitor of PI3K, inhibits the proliferation and migration of RSC96 cells. Further studies have found that DHI can also promote the expression of CXCL12 and GDNF at gene and protein levels, and CXCL12 is, while GDNF is not, PI3K/AKT pathway-dependent. Animal experiments also confirmed that DHI could promote CXCL12 and GDNF expression and promote facial nerve function recovery and myelin regeneration. In conclusion, our in vitro and in vivo experiments demonstrated that DHI could promote the proliferation and migration of Schwann cells through the PI3K/AKT pathway and increase the expression of CXCL12 and GDNF to promote facial nerve function repair.