Friction and wear properties of hot working die steel at above 800 °C are of particular interest for high temperature applications. Here, novel AlCoCrFeNiWx high-entropy alloy (HEA) coatings have been fabricated on the surface of hot working die steel by laser cladding. The effects of the as-prepared AlCoCrFeNiWx HEA coatings on the microstructure and high temperature friction and wear behavior of hot working die steel are investigated through scanning electron microscopy (SEM), electron probe microanalysis (EPMA), X-ray diffraction (XRD), and X-ray absorption fine structure (XAFS). Having benefited from the formation of W-rich intermetallic compounds after the addition of W elements, the high temperature wear resistance of the coatings is obviously improved, and friction coefficient shows a large fluctuation. The microstructural characteristics of the AlCoCrFeNiWx HEA coatings after the high temperature wear resistance test shows a highly favorable impact on microstructure stability and wear resistance, due to its the strong lattice distortion effect of W element on BCC solid solutions and the second phase strengthening of the W-rich intermetallic compounds. These findings may provide a method to design the high temperature wear resistant coatings.

Recently, cold-adaptation medicine has gotten more and more attention because of its specific significance to health care, military activities, sports performance, and so on. Although numerous studies have focused on respiratory, immune, and circulatory systems as well as skin damage upon cold exposure, the impacts on central nervous system are not well understood. This study explores the effects of chronic cold exposure on the murine central nervous system. To establish a chronic cold-exposure animal model, adult male mice from postnatal days 40-50 (P40-50) were housed at 0-4°C for 20 days. During the study period, estrogen receptors were labeled via immunohistochemistry, the dendritic spines of visual cortical pyramidal cells were labeled with DiI diolistic assay, and synaptic ultrastructure was observed by transmission electron microscopy. The results showed that cold exposure could inhibit neural proliferation significantly, with an increase of G-protein-coupled receptor 30 (GPR30) expression. Chronic cold exposure could also induce a decrease in the dendritic spines of pyramidal cells in visual cortex, along with a decrease in the number of synaptic formations. The ultrastructure of synapses after cold exposure was observed. It was found that pre- and postsynaptic membranes were fused, with a vague synaptic cleft. Furthermore, neuronal cytoplasmic and organelle swellings were also observed, along with microtubule disintegration. In conclusion, chronic cold exposure can cause structural and functional changes in the mouse central nervous system, possibly by direct participation of estrogen and its receptor, GPR30, in response to chronic cold exposure.