Failure mechanism of bolting support and high-strength bolt-grouting technology for deep and soft surrounding rock with high stress

In deep underground mining, the surrounding rocks are very soft with high stress. Their deformation and destruction are serious, and frequent failures occur on the bolt support. The failure mechanism of bolt support is proposed to solve these problems. A calculation theory is established on the bond strength of the interface between the anchoring agent and surrounding rocks. An analysis is made on the influence law of different mechanical parameters of surrounding rocks on the interfacial bond strength. Based on the research, a new high-strength bolt-grouting technology is developed and applied on site. Besides, some helpful engineering suggestions and measures are proposed. The research shows that the serious deformation and failure, and the lower bond strength are the major factors causing frequent failures of bolt support. So, the bolt could not give full play to its supporting potential. It is also shown that as the integrity, strength, interface dilatancy and stress of surrounding rocks are improved, the bond strength will increase. So, the anchoring force on surrounding rocks can be effectively improved by employing an anchoring agent with high sand content, mechanical anchoring means, or grouting reinforcement. The new technology has advantages in a high strength, imposing pre-tightening force, and giving full play to the bolt supporting potential. Hence, it can improve the control effect on surrounding rocks. All these could be helpful references for the design of bolt support in deep underground mines.

ADAR1 regulates vascular remodeling in hypoxic pulmonary hypertension through N1-methyladenosine modification of circCDK17

Pulmonary hypertension(PH)is an extremely malignant pulmonary vascular disease of unknown etiology.ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine,thereby affecting RNA expression.However,the role of ADAR1 in PH development remains unclear.In the present study,we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling.Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells(PASMCs).Conversely,inhibition of ADAR1 produced opposite effects.High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH.CircCDK17 level was significantly lowered in the serum of PH patients.The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17.ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from mlA modification.We demonstrate for the first time that ADAR1 contributes to the PH development,at least partially,through m1A modification of circCDK17 and the subsequent PASMCs proliferation.Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.

Expression of airway mucus-associated proteins in rats with chronic obstructive pulmonary disease with a cold-dryness symptom pattern

OBJECTIVE: To reveal the effects on expression of airway mucus-associated proteins in rats with chronic obstructive pulmonary disease(COPD) and a cold-dryness symptom pattern induced by elastase and smoking.METHODS: The COPD model was established with an elastase dose into the trachea combined with exposure to smoking; the COPD model cold-dryness symptom pattern was further developed by exposure to a cold, dry environment. After 90 days,pathologic lung sections, inflammatory cytokine levels(measured by enzyme linked immunosorbent assay), m RNA and protein expression of mucus-associated proteins and aquaporins(measured by real-time polymerase chain reaction and western blots) were examined.RESULTS: Cytokines interleukin-6(IL-6), interleukin-8(IL-8), and tumor necrosis factor-α(TNF-α) in the COPD and the cold-dryness symptom pattern COPD groups were all significantly higher than in controls(each P < 0.01). IL-6 and IL-8 levels were higher in the cold-dryness symptom pattern COPD group than in the COPD group(each P < 0.05). The AQP5 m RNA expression in the cold-dryness symptom pattern COPD and COPD groups was lower than in the control group(P < 0.01), and that in the cold-dryness symptom pattern COPD group was lower than the COPD group(P < 0.05). The expression of MUC5 AC and MUC5 B m RNAs in the cold-dryness symptom pattern COPD group and COPD group was higher than in the control group(each P < 0.01), and that in the cold-dryness symptom pattern COPD group was higher than the COPD group(P < 0.01, and P < 0.05, respectively).The ratio of MUC5 AC m RNA/MUC5 B m RNA was COPD group < the cold-dryness symptom pattern COPD group < the control group. AQP4 and AQP5 protein expression in the cold-dryness symptom pattern COPD group was lower than that in the COPD group which was lower again than in the control group. MUC5 AC and MUC5 B expression in the cold-dryness symptom pattern COPD group was higher than in the COPD group and higher again than in the control group.CONCLUSION: Cold-dryness affects the expression of mucus-associated protein m RNA and its corresponding proteins, reducing the secretion of aquaporins and increasing the secretion of mucins. Imbalance in aquaporins and mucins can affect the function of mucus, increasing airway obstruction.