The strip filling mining method can solve the problems related to mining under structures, under aquifers, and under infrastructure (3U coal seams), while the reasonable selection of the mining and filling sequence still requires further investigation. The current study was conducted to investigate the stress and surface subsidence of a filling body (or coal pillar) under two filling sequences through theoretical analysis, similar simulation tests, and numerical simulations. To achieve optimal filling materials for the Liudong Coal Mine, a low-strength similar paste filling material composed of fly ash, gypsum, and sand was developed. The relationships between the strength and the cement ratio and between the strength and the sand-binder ratio were discussed. Similar simulation tests showed that mining scheme 1 (mining before filling) could lead to the formation of an isolated island coal pillar in the mining process, mining scheme 2 (filling before mining) had less influence on surface subsidence, and the stress on the filling body was smaller for scheme 2 than for scheme 1. The distributions of the stress and plastic zone in the two different mining and filling sequences were obtained through numerical simulations. The method of first filling and then mining could greatly reduce the stress concentration and plastic zone during the mining process. In summary, mining scheme 2 (filling before mining) can avoid the formation of isolated island coal pillars in the process of mining, and without considering other factors, scheme 2 should be adopted as much as possible.

Interleukin-25 (IL-25) is an important regulatory cytokine that has a key role on mucosal immune tolerance during inflammation response. However, the molecular mechanism that regulates the colonic IL-25 expression in Crohn's disease (CD) remains unclear. In this study, IL-25 level was proved to decrease in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis mice and IL-10 knockout (KO) spontaneous colitis mice. An inverse correlation between IL-25 and miR-31 was discovered in the colons from model mice and CD patients. Furthermore, target validation analysis demonstrated that miR-31 directly regulated IL-25 expression by binding to its messenger RNA 3'-untranslated region. Changing colonic miR-31 level in the colitis mice could affect the mucosal IL-12/23-mediated Th1/Th17 pathway and lead to either amelioration or aggravation of colonic inflammation. In addition, the therapeutic effects of anti-miR-31 in TNBS-induced colitis were abolished by colonic treatment with IL-25 antibody or colonic down-expression of IL-25. Our findings demonstrated that IL-25 could be a crucial anti-inflammatory cytokine in TNBS-induced colitis and the signaling of miR-31 targeting IL-25 might be a possible mechanism that regulates IL-12/23-mediated Th1/Th17 inflammatory responses during colonic inflammation process. Restoring colonic IL-25 expression and blocking Th1/Th17 responses via intracolonic administration of miR-31 inhibitor may represent a promising approach for CD treatment.

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