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In order to investigate the distribution patterns of in situ stress in the main coal seams (3# and 15#) of the Qinshui coalfield, an in-depth analysis was conducted on the in situ stress measurement results obtained from 139 measurement points across 46 mines within the mining area. The findings indicate that the maximum horizontal principal stress in the coal mining area of both seams is generally higher than the vertical principal stress. The stress field exhibits characteristics of a tectonic stress field, while deeper regions display features of a vertical stress field. The in situ stress values in the mining area of coal seam 3# are predominantly characterized by moderate stress field zones, while those in the mining area of coal seam 15# are mainly composed of low to moderate stress field zones. The maximum horizontal principal stress in the Yangquan and Changzhi mining areas for both coal Seams 3# and 15# is concentrated in the NE direction, whereas in the Jincheng mining area, it is predominantly concentrated in the NW direction, indicating a clear directionality. With increasing depth, the following trends can be observed approximately: the maximum and minimum horizontal principal stress values generally exhibit an increasing trend, and the geological structures throughout the mining area are primarily dominated by horizontal tectonic movements; the lateral pressure ratio gradually decreases and tends to concentrate near the value of 1; the relative difference between the maximum and minimum principal stresses tends to increase, with the horizontal principal stress difference ratio concentrating near 0.5. The relationship between the average horizontal principal stress ratio (k) and vertical principal stress at different depths within the measured area follows Hawke-Brown’s general law for this relationship curve. The research results have important guiding significance for the design of coal mining engineering in this area.

This paper presents a new approach for damage detection in thin plates by fusing variational mode decomposition and spectral entropy (VMD-SE). In this method, after the received signal is decomposed into some intrinsic mode functions (IMFs) by variational mode decomposition (VMD), the spectral entropy ratio of the first and last IMFs is calculated for optimizing the VMD's parameters and improving its decomposition performance. Moreover, the cross-correlation coefficient between the decomposed IMFs and the reference signal is computed to separate the desired IMF, which contains more damage information. Finally, the spectral entropy of the obtained IMF is calculated as an indicator for assessing the damage's severity. The comparative analysis of the simulated signal clearly shows that only the proposed method can successfully separate the damage-related and reference signals. To verify the VMD-SE method, damage detection of two different types of damage on aluminum and composite fiber-reinforced polymer (CFRP) plates is conducted by using this new approach. The experimental results demonstrate that the parameters of VMD affect greatly its decomposition performance, and the best parameters are selected. The results also indicate that the normalized spectral entropy monotonically increases when the diameter of the through-hole or the length of the scratch increases. In addition, the correlation coefficients of the fitting lines of the plates are larger than 0.998. The experimental results of aluminum specimens demonstrate that the damage's location has an influence on the normalized spectral entropy. At last, based on the linear relationship, the severity of damage in the fourth specimen is identified. The identification results demonstrate that the relative error of the aluminum and CFRP plates is less than 7.34%, which indicates that this new algorithm by fusing VMD and spectral entropy can detect the damage size in thin plates accurately and efficiently. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m6A) serves a critical role in regulating gene expression and has been associated with various diseases; however, its role in the differentiation of endothelial progenitor cells (EPCs) remains unclear. The present study used liquid chromatography with tandem mass spectrometry and immunofluorescence assays to quantify the levels of m6A in human peripheral blood-derived EPCs (HPB-EPCs) before and after differentiation into mature cells. The present study performed Cell Counting Kit 8, Transwell, and tube formation assays to determine the effects of overexpression and knockdown of Wilms' tumor 1-associated protein (WTAP) on HPB-EPCs. The results revealed that the level of m6A modification was significantly increased during HPB-EPCs differentiation, and WTAP exhibited the most significant alteration among the enzymes involved in m6A regulation. When WTAP was overexpressed in HPB-EPCs, cell proliferation, invasion, and the formation of tubes were improved, whereas WTAP knockdown yielded the opposite effects. In conclusion, the present study highlighted the involvement of m6A in regulating EPC differentiation, with WTAP acting as a promoter of EPC differentiation. [ABSTRACT FROM AUTHOR]

• GAE is an alternative for patients with osteoarthritis (OA) related knee pain that is refractory to conservative treatment. • GAE was effective in treating knee pain secondary to mild to severe OA, but less improvement was observed in the severe group. • More comparative research needs to be conducted before reliable inferences about the effectiveness of GAE can be made. To evaluate the safety and efficacy of genicular artery embolization (GAE) in patients with mild-to-severe knee osteoarthritis up to 12 months after GAE. This prospective single-center study included patients who had knee osteoarthritis for >1 year with moderate-to-severe pain after failed conservative treatment for >6 months. Baseline imaging features were evaluated to determine Kellgren-Lawrence (KL) grade and magnetic resonance imaging (MOAKS) scores. GAE was performed using 150–350 μm embolic polyvinyl alcohol particles. The visual analog scale (VAS) and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores were used to evaluate knee pain, stiffness, and function at baseline and follow-up. The primary endpoints were changes in VAS and WOMAC scores at 12 months. Thirty-three patients (n = 37 knees) aged 66.6 ± 8.7 years were enrolled. The patients were categorized into two groups: mild-to-moderate osteoarthritis (n = 28, KL grades 2–3) and severe osteoarthritis (n = 9, KL grade 4). GAE was successfully performed in all patients, with no major adverse events. Three to six branches of the genicular artery were embolized. The mean VAS and WOMAC scores in the mild-to-moderate group significantly decreased (6.6 at baseline vs. 3.0 at 12 months and 49.4 vs. 27.4, respectively, all P < 0.001). The mean VAS and WOMAC scores in the severe group significantly decreased at 12 months (7.3 vs. 4.4 and 58.1 vs. 40.6, respectively, all P < 0.001). GAE is a well-tolerated and effective treatment that significantly improves pain symptoms and function in patients with mild-to-severe knee osteoarthritis. [ABSTRACT FROM AUTHOR]

Estrogen Receptor 2 (ESR2) is the protein-coding gene of estrogen receptor β (ERβ) and has been shown to be abundantly expressed in gastric carcinoma (GC), suggesting that it plays a role in GC pathogenesis. However, the underlying molecular mechanism remains elusive. In the present in vitro study, GC cell growth was found to be estrogen-dependent, and the expression level of ERβ was higher than that of ERα. Knocking down the endogenous expression of ESR2 in GC cells increased the apoptosis rate and the level of cleaved caspase-3, caspase-7 and poly ADP-ribose polymerase. The induced apoptosis was primarily related to GC cell growth arrest, accompanied with activation of DNA damage-inducible protein 45 alpha (GADD45α) in a p53-independent manner. Importantly, down-regulation of ESR2 also promoted autophagy. The autophagy inhibitor 3-MA or silencing ATG7 rescued the apoptosis by knocking down ESR2 via activation of the MAPK signaling pathway in AGS cells, leading to increased apoptosis. In conclusion, these results demonstrated that suppression of ESR2 gene expression could promote GC cell apoptosis, suggesting that it may prove to be a potential therapeutic target for GC., Competing Interests: None., (AJTR Copyright © 2020.)