Coal Wall Spalling Mechanism and Grouting Reinforcement Technology of Large Mining Height Working Face

To control the problem of coal wall spalling in large mining height working faces subject to mining, considering the Duanwang Mine 150505 fully mechanized working face, the mechanism of coal wall spalling in working faces was investigated by theoretical analysis, numerical simulation and field experiment. Based on analysis of coal wall spalling in the working face, a new grouting material was developed. The stress and plastic zone changes affecting the coal wall, before and after grouting in the working face, were analyzed using numerical simulation and surrounding rock grouting reinforcement technology was proposed for application around the new grouting material. The results showed that: (1) serious spalling of the 150505 working face was caused by the large mining height, fault influence and low roof strength, and (2) the new nano-composite low temperature polymer materials used have characteristics of rapid reaction, low polymerization temperature, adjustable setting time, high strength and environmental protection. Based on analysis of the working face coal wall spalling problem, grouting reinforcement technology based on new materials was proposed. Industrial tests were carried out on the working face. Field monitoring showed that the stability of the working face coal wall was significantly enhanced and that rib spalling was significantly improved after comprehensive anti-rib-spalling grouting measures were adopted. These results provide a basis for rib spalling control of working faces under similar conditions

In Vivo Delivery of Adenoviral Vector Containing Interleukin-17 Receptor A Reduces Cardiac Remodeling and Improves Myocardial Function in Viral Myocarditis Leading to Dilated Cardiomyopathy

<div><p>Th17 cells have been implicated in the pathogenesis of myocarditis. Interleukin (IL)-17A produced by Th17 cells is dispensable for viral myocarditis but essential for the progression to dilated cardiomyopathy (DCM). This study investigated whether the adenoviral transfer of the IL-17 receptor A reduces myocardial remodeling and dysfunction in viral myocarditis leading to DCM. In a mouse model of Coxsackievirus B3 (CVB3)-induced chronic myocarditis, the delivery of the adenovirus-containing IL-17 receptor A (Ad-IL17RA:Fc) reduced IL-17A production and decreased the number of Th17 cells in the spleen and heart, leading to the down-regulation of systemic TNF-α and IL-6 production. Cardiac function improved significantly in the Ad-IL17R:Fc- compared with the Ad-null-treated mice 3 months after the first CVB3 infection. Ad-IL17R:Fc reduced the left ventricle dilation and decreased the mortality in viral myocarditis, leading to DCM (56% in the Ad-IL17R:Fc versus 76% in the Ad-null group). The protective effects of Ad-IL17R-Fc on remodeling correlated with the attenuation of myocardial collagen deposition and the reduction of fibroblasts in CVB3-infected hearts, which was accompanied by the down-regulation of A distintegrin and metalloprotease with thrombospondin type 1 motifs (ADAMTS-1), Matrix metalloproteinase-2(MMP-2), and collagen subtypes I and III in the heart. Moreover, in cultured cardiac fibroblasts, IL-17A induced the expression of ADAMTS-1, MMP-2, and collagen subtypes I and III and increased the proliferation of fibroblasts. We determined that the delivery of IL-17-RA:Fc reduces cardiac remodeling, improves function, and decreases mortality in viral myocarditis leading to DCM, possibly by suppressing fibrosis. Therefore, the adenoviral transfer of the IL-17 receptor A may represent an alternative therapy for chronic viral myocarditis and its progression to DCM.</p></div

The levels of IL-6 and TNF-α in the supernatants of cardiac fibroblast cultures treated with IL-17.

<p>The IL-17 (10 ng/ml)-treated group produced higher levels of IL-6 and TNF-α cytokines than the control- and IL-17 (5 ng/ml)-treated groups. Moreover, IL-6 in the IL-17 (5 ng/ml)-treated group was highly expressed in the supernatants of the heart homogenates (ELISA). The values in the IL-17-treated CFs were normalized to the values in the control cells (n = 5 per group). The data represent the mean ± SEM. **<i>P</i><0.01 vs control group, ^##<i>P</i><0.01 vs control group.</p

Degradation of CFs related to the MMPs/TIMPs expression following neutralization of IL-17.

<p>(<i>A</i>) Representative western blots showing the expression of the cardiac ADAMTS-1 protein in each group. (<i>B</i>) Representative western blots showing the expression of the cardiac TIMP-1 protein in each group. (<i>C</i>) Representative western blots showing the expression of the cardiac MMP-2 protein in each group. The expression of the cardiac ADAMTS-1 and MMP-2/TIMP-1 proteins in each group is expressed as a ratio of the GAPDH expression for the same sample. On day 90, 3 mice per group were analyzed. *<i>P</i><0.05 vs control group.</p