According to the on-site vibration velocity monitoring and peak vibration velocity prediction, it is found that the maximum vibration velocity generated by the existing Dizong blasting scheme does not meet the requirements of the maximum allowable vibration velocity of houses. Therefore, the existing blasting scheme is optimized by reducing the maximum single-segment charge and a variety of damping measures such as multistage duplex wedge groove, adding damping hole, and millisecond blasting. In addition, the blasting data before and after optimization are analyzed and compared by wavelet (packet) technology. The results show that the optimized blasting main frequency domain is increased to 50∼150 Hz and the maximum vibration intensity value is reduced by 79.8%. Based on the time-energy analysis, the maximum energy value is reduced by 67.75% compared with the original scheme, and the dominant energy of the original scheme is reduced by 97.81%, 71.49%, 82.44%, 95.93%, and 93.03%, respectively, after optimization. The maximum vibration velocity generated by the optimized blasting scheme construction is 1.12 cm/s, which is less than the maximum allowable vibration velocity of the building of 1.2 cm/s, which meets the maximum allowable vibration velocity requirements of the building. The optimized blasting scheme realizes the safe and rapid construction of the two steps of the Dizong tunnel, which can provide a reference for similar engineering construction in the future.
This paper takes the Dizong tunnel engineering as its background. Combined with the on-site monitoring data, the wavelet packet program based on MATLAB was compiled to study the vibration response of the four-story masonry building in a typical southwestern mountainous area of China under the blasting load. The results showed that the maximum particle velocity increased to the 3rd floor and attenuation occurred on the 4th floor. The particle velocity in the z-direction was the largest and should be paid attention. The dominant frequency of the building showed a trend from high frequency to low frequency, the duration became short, and the acceleration decreased to the 4th floor. With the increase of the building floor, the main frequency domain of the building decreased and then gradually tended to the low-frequency domain. The high-frequency particle velocity gradually decreased, gathered to the low frequency, and developed from the dispersed multiband to the concentrated low-frequency band. The total energy value of vibration increased to the 3rd floor and then decreased to the 4th floor. The energy of the building was between 0 and 171.6 Hz. The higher the floor was, the more concentrated the energy was in the low-frequency domain.
Cadmium is a toxic heavy metal which could cause central nervous system damage and cognitive dysfunction. However, the effective therapy strategy for cadmium-caused cognitive dysfunction had not been established. In present study, we investigated the therapeutic effect of artesunate on cadmium induced cognitive deficits and neural stem/progenitor cells (NSPCs) proliferation as well as neurogenesis inhibition. Male mice were injected with cadmium chloride (1mg/Kg) for 4weeks, followed with 4 weeks of artesunate (50mg/Kg). Cadmium chloride and artesunate were used to treat NSPCs in vitro. Subsequently, the learning and memory function of mice were detected by Y-maze and Morris water maze tests and NSPCs proliferation and neurogenesis were examined by western blots and immunofluorescence. The results showed cadmium impaired mice cognitive severity. And cadmium significantly inhibited the proliferation and neurogenesis of NSPCs in hippocampi and in vitro. Moreover, cadmium reduced the expression of phosphorylated AKT. However, artesunate reversed the cadmium-induced cognitive deficits as well as the inhibition of NSPCs proliferation and neurogenesis. Additionally, artesunate increased the phosphorylation of AKT in hippocampi and NSPCs. Our data manifested artesunate could reverse cadmium-induced mice cognitive deficits and reduce the inhibition of cadmium on NSPCs proliferation and neurogenesis via PI3K-AKT pathway.
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