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The Ⅵ-22080 working face of Pingmei No.8 mine was selected as the research object. Through FLAC3D numerical simulation method, the stress evolution characteristics of the working face were analyzed, and the working face was divided into regions. The results show that the stress distribution of working face has a great difference under the joint influence of large spacing coal pillar of group Ⅳ coal seam and the coal seam mining of group Ⅴ coal seam. Stress concentration phenomenon is distributed in the whole haulage roadway, especially in the range of 150 m to 500 m from the outer entrance of the roadway. The maximum vertical stress of the roadway is 27.5 MPa, increased by 8 MPa. There is a pressure relief zone near the air-return roadway of the working face and the maximum pressure relief degree is 10 MPa. With the increase of stress, the fracture rate and permeability of coal decrease by 29 % and 64% respectively. In the high stress superimposed area, the gas pressure gradient increases, the permeability of coal body decreases, and the outburst risk increases. On the contrary, the permeability of coal seam in the pressure relief zone increases, and the outburst risk is smaller. According to the difference of outburst risk in different areas of working face, the working face can be divided into general outburst risk area, medium outburst risk area and severe outburst risk area.

Background: Prenatal alcohol exposure (PAE) has been linked to congenital heart disease and fetal alcohol syndrome. The heart primarily relies on mitochondria to generate energy, so impaired mitochondrial function due to alcohol exposure can significantly affect cardiac development and function. Our study aimed to investigate the impact of PAE on myocardial and mitochondrial functions in offspring mice. Methods: We administered 30% alcohol (3 g/kg) to pregnant C57BL/6 mice during the second trimester. We assessed cardiac function by transthoracic echocardiography, observed myocardial structure and fibrosis through staining tests and electron transmission microscopy, and detected cardiomyocyte apoptosis with dUTP nick end labeling assay and real‐time quantitative PCR. Additionally, we measured the reactive oxygen species content, ATP level, and mitochondrial DNA copy number in myocardial mitochondria. Mitochondrial damage was evaluated by assessing the level of mitochondrial membrane potential and the opening degree of mitochondrial permeability transition pores. Results: Our findings revealed that PAE caused cardiac systolic dysfunction, ventricular enlargement, thinned ventricular wall, cardiac fibrosis in the myocardium, scattered loss of cardiomyocytes, and disordered arrangement of myocardial myotomes in the offspring. Furthermore, we observed a significant increase in mitochondrial reactive oxygen species content, a decrease in mitochondrial membrane potential, ATP level, and mitochondrial DNA copy number, and sustained opening of mitochondrial permeability transition pores in the heart tissues of the offspring. Conclusions: These results indicated that PAE had adverse effects on the cardiac structure and function of the newborn mice and could trigger oxidative stress in their myocardia and contribute to mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]