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Abstract Rock bursts in roadway groups of deep mining workfaces are more likely to occur due to concentrated static loads, posing significant threats to mining safety and efficiency. In this study, the coal mine roadway groups in western China are taken as an engineering case to investigate the occurrence mechanism of rock bursts in deep mining workfaces caused by concentrated static loads. A novel prevention and control method based on hydraulic fracturing is proposed, and a sensitivity analysis is conducted on key parameters, including in-situ stress, roof firmness coefficient, flow increment, and borehole spacing, to assess their influence on the hydraulic fracturing effect. The results reveal that the failure energy and peak stress of coal pillars within the roadway group gradually increase due to the continuous pressure exerted by the overlying roof, eventually reaching the conditions necessary to trigger rock bursts. The application of a super-long horizontal staged hydraulic fracturing technology transforms the thick, hard roof into a plastic cushion, which absorbs energy and weakens the stress transfer from the overlying roof. This process effectively reduces the stress concentration in the coal pillars. Furthermore, the hydraulic fracturing effect improves with increasing in-situ stress difference and decreasing borehole spacing, while the effect of flow increment is relatively limited. The study also highlights that higher roof firmness coefficients hinder the effectiveness of hydraulic fracturing, as greater water pressure is required for fracture propagation. Field application of the hydraulic fracturing technique, with parameters including an in-situ stress difference (λ), rock strata firmness coefficient, flow rate of 50 m3/day, borehole spacing of 60 m, and a borehole horizontal level of 40–50 m above the roadway, led to a significant reduction in microseismic events and ground audio frequency, demonstrating a remarkable anti-impact effect on-site. This research provides a theoretical framework and practical insights for the prevention and mitigation of concentrated static load-induced rock bursts in similar mining roadway groups.

Abstract The transition between the planktonic state and the biofilm-associated state is a key developmental decision for pathogenic bacteria. Biofilm formation by Yersinia pestis is regulated by hmsHFRS genes (β-1, 6-N-acetyl-D-glucosamine synthesis operon) in its flea vector and in vitro. However, the mechanism of biofilm formation in Yersinia pseudotuberculosis remains elusive. In this study, we demonstrate that the LysR-type regulator RovM inversely regulates biofilm formation and motility in Y. pseudotuberculosis by acting as a transcriptional regulator of these two functions. RovM is strongly induced during growth in minimal media but strongly repressed in complex media. On one hand, RovM enhances bacterial motility by activating the expression of FlhDC, the master regulator of flagellar genes, via the recognition of an operator upstream of the flhDC promoter. On the other hand, RovM represses β-GlcNAc production under nutrition-limited conditions, negatively regulating hmsHFRS expression by directly binding to the −35 element of its promoter. Compared to wild-type bacteria, the rovM mutant established denser biofilms and caused more extensive mortality in mice and silkworm larvae. These results indicate that RovM acts as a molecular switch to coordinate the expression of genes involved in biofilm formation and motility in response to the availability of nutrients.