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• Support mechanisms for thin spray-on liners (TSLs) are summarized. • The effect of high humidity on the bond of TSLs to granite is investigated. • Bond failure modes at the TSLs-granite interface were analyzed. • The effect of high humidity on the mechanical properties of TSLs was studied. • The pore structure of TSLs at high humidity was observed. Thin Spray-on Liners (TSLs) are a novel rock support technology used in underground projects, which often encounter harsh environments such as high humidity. The mechanical properties of TSLs are affected by the high humidity environment. This study aims to summarize the support mechanisms of TSLs and evaluate the effects of humidity on their performance. Two cement-based TSLs were prepared. They used vinyl acetate-ethylene copolymer emulsion (VAE emulsion) and polyacrylate emulsion as modifying materials, respectively. Specimens were subjected to four different humidity environments for 7 days. The mechanical properties of the specimens were evaluated through compressive, flexural and pull-out tests. The impermeability test was utilized to test the sealing of TSLs. Microscopic observation was conducted using a Lecia microscope. The study also analyzed the interfacial failure modes observed in the pull-out test. The results indicated that increasing humidity hindered the film formation reaction of TSLs, preventing the formation of a continuous three-dimensional spatial polymer mesh structure. Instead, cohesive large particles were formed, negatively impacting the mechanical properties. Additionally, increasing humidity led to the formation of large pores and crack lines within TSLs, further decreasing their mechanical and sealing properties. The increase in humidity also weakened the dry shrinkage effect of TSLs, resulting in increased bond strength. Therefore, analyzing the initial mechanical properties of TSLs under high humidity conditions is crucial for guiding their application in underground projects. [ABSTRACT FROM AUTHOR]

• BMSC-EVs can be delivered to macrophages and miR-17 expresses highly in BMSC-EVs. • MiR-17 carried by BMSC-EVs reduces the LPS-induced macrophage inflammation. • MiR-17 carried by BMSC-EVs reduces the sepsis response in mice. • MiR-17 carried by BMSC-EVs regulates EZH2/TRAIL axis via BRD4. • MiR-17 carried by BMSC-EVs might provide a novel therapy for sepsis. Sepsis, as a disease affecting the microcirculation and tissue perfusion, results in tissue hypoxia and multiple organ dysfunctions. Bone mesenchymal stem cell (BMSC)-derived extracellular vesicles (EVs) have been demonstrated to transfer trivial molecules (proteins/peptides, mRNA, microRNA and lipids) to alleviate sepsis. We sought to define the function of microRNA (miR)-17 carried in BMSC-EVs in sepsis. The purity of the extracted BMSCs was identified and confirmed by detection of the surface markers by flow cytometry, followed by osteoblastic, adipogenic, and chondrocyte differentiation experiments. Subsequently, EVs were collected from the medium of BMSCs. The uptake of PKH-67-labeled BMSC-EVs or EVs carrying cy3-miR-17 by RAW264.7 cells was observed under laser confocal microscopy. Furthermore, a series of gain- and loss-of-function approaches were conducted to test the effects of LPS, miR-17 and BRD4 on the inflammatory factors (IL-1β, IL-6 and TNF-α), number of M1 macrophages and M2 macrophages, inflammatory-related signal pathway factors (EZH2, c-MYC and TRAIL), macrophage proliferation, and apoptosis in sepsis. The survival rates were measured in vivo. BMSC-EVs was internalized by the RAW264.7 cells. BDR4 was verified as a target of miR-17, while the expression pattern of miR-17 was upregulated in BMSC-EVs. MiR-17 carried by BMSC-EVs inhibited LPS-induced inflammation and apoptosis of RAW264.7 cells, but improved the viability of RAW264.7 cells. Next, in vitro experiments supported that miR-17 inhibited LPS-induced inflammation in RAW264.7 cells through BRD4/EZH2/TRAIL axis. BRD4 overexpression reversed the effects of miR-17. Moreover, the therapeutic function of BMSC-EVs carried miR-17 was verified by in vivo experiments. MiR-17 derived from BMSCs-EVs regulates BRD4-mediated EZH2/TRAIL axis to essentially inhibit LPS-induced macrophages inflammation. [ABSTRACT FROM AUTHOR]