Research on Improving Moisture Resistance of Asphalt Mixture with Compounded Recycled Metallurgical Slag Powders.

The utilization of steel slag as an alternative material in asphalt mixtures is considered the solution to the problem of the shortage of natural aggregates. However, asphalt mixtures with steel slag show susceptibility to damage caused by moisture, especially in powder form. Therefore, blast furnace slag powders were used to compound with steel slag powders as fillers to improve the moisture resistance of asphalt mixtures. The characteristics of the steel slag powders and blast furnace slag powders were investigated initially. Subsequently, the adhesion properties of the asphalt mastics with the powders to the aggregates were evaluated. Finally, the moisture resistances of the asphalt mixtures were identified. The results indicate that the steel slag powder exhibited a notable prevalence of surface pores, which had a more uniform size distribution. In contrast, the blast furnace slag powder exhibited a greater average pore size. The larger specific surface area of the steel slag powder was over 30% larger than that of the blast furnace slag powder, and the superior gelling activity of the blast furnace powder enhanced the adhesion property. Both the steel slag powder and blast furnace slag powder were found to enhance the adhesion properties of the asphalt mastics, while the effect of the steel slag powder was more pronounced, the maximum force difference of which exceeded 200 N. The antagonistic effect of the steel slag powder and blast furnace slag powder on the resistance of the adhesive interface to moisture damage was confirmed by the contact angle test. The incorporation of the blast furnace slag powder markedly enhanced the moisture resistances of the asphalt mixtures. The phenomenon of dynamic moisture damage to the asphalt mixtures was more pronounced under the multicycle times, obviously severer than that in a stable water environment. As the dynamic moisture cycles increased, the degree of destruction gradually approached a steady state.

Poly-(lactic acid) composite films comprising carvacrol and cellulose nanocrystal-zinc oxide with synergistic antibacterial effects.

Herein, carvacrol (CRV) and modified cellulose nanocrystal-zinc oxide (CNC-ZnO) were incorporated into a poly (lactic acid) (PLA) matrix to prepare a PLA-based composite film using a simple solution casting method to achieve antimicrobial effects for application in antimicrobial food packaging. Compared with films obtained from neat PLA, the PLA@CRV20%@CNC-ZnO3% composite film shows better performance in terms of mechanical properties, ultraviolet (UV) blocking, and antimicrobial effects. The PLA composites containing CRV and 3 wt% CNC-ZnO blends exhibit improved tensile strength (21.8 MPa) and elongation at break (403.1 %) as well as excellent UV resistance. In particular, CRV and the CNC-ZnO hybrid endow the obtained PLA composite films with a synergistic antibacterial effect, resulting in good antibacterial properties for microbes, such as Escherichia coli, Staphylococcus aureus and Aspergillus niger. The diameters of the inhibition zone of the PLA@CRV20%@CNC-ZnO3% composite films against E. coli, S. aureus, and A. niger were 4.9, 5.0, and 3.4 cm, respectively. Appling the PLA@CRV20%@CNC-ZnO3% composite film as an antibacterial food packaging material, the storage period for strawberries was considerably extended. This study provides a theoretical basis for developing new organic/inorganic composite antimicrobial film materials from PLA.

Long noncoding RNA PVT1 inhibits interferon-α mediated therapy for hepatocellular carcinoma cells by interacting with signal transducer and activator of transcription 1.

Long noncoding RNA (LncRNA) PVT1 has recently been reported to be involved in the development of hepatocellular carcinoma (HCC) and hsigh expression of oncogenic PVT1 is associated with poor prognosis of HCC. Interferon-α (IFN-α) has been used in clinic for HCC therapy. However, whether PVT1 is involved in the IFN-α therapy for HCC is completely unknown. Our study found that high PVT1 expression in HCC cells is associated with high unmethylation in PVT1 promoter region. IFN-α treatment further increases PVT1 expression in HCC cells by enhancing H3K4me3 modification on the promoter. Furthermore, PVT1 knockdown enhances IFN-α-induced HCC cell apoptosis by promoting phosphorylation of signal transducer and activator of transcription 1 (STAT1) and upregulating IFN-stimulated genes expression. Moreover, PVT1 specifically interacts with STAT1 in HCC cells. Taken together, these results for the first time indicate that IFN-α treatment promotes oncogenic PVT1 expression in HCC cells, which interacts with STAT1 to inhibit IFN-α signaling, ultimately blocking IFN-α-induced cells apoptosis, suggesting that lncRNA PVT1 may be a potential target to improve IFN-α-mediated HCC immunotherapies.