Monitoring warning criterion of acoustic emission active waveguide system based on loess deformation and failure.

The construction of acoustic emission criterion system is crucial for monitoring and providing early warning of geological hazards. In the current soil acoustic emission monitoring methods, the signal generated by soil deformation and failure is weak and experiences high attenuation, resulting in a low level of the monitored signal. One approach to enhance the quality of monitoring data is by utilizing the active waveguide model. However, the current research on the active waveguide model system is not extensive. To address these issues, a set of active waveguide system was designed to improve the data quality of acoustic emission monitoring and early warning. The deformation and failure process of loess monitored by acoustic emission was divided into stages, and the precursor information of acoustic emission for geological disasters in loess areas was comprehensively deconstructed. The data quality advantage of the active waveguide model was verified through comparative experiments of with the passive waveguide model. This study investigates the AE signal characteristics of the active waveguide model. It explores various aspects such as the AE waveform parameter characteristics, the discrimination method for failure mode based on RA-AF value, the AE r-value characteristics, the AE b-value characteristics, and the frequency-amplitude characteristics. The study reveals the evolution law of AE signals in the active waveguide model, including early warning signs and failure morphological characteristics. Furthermore, it constructs a warning criterion for the active waveguide system. The development of this criterion system is of great importance in guiding the monitoring and early warning of geological disasters in loess areas.

The RagA GTPase protects young egg chambers in Drosophila.

The preservation of female fertility under unfavorable conditions is essential for animal reproduction. Inhibition of the target of rapamycin complex 1 (TORC1) is indispensable for Drosophila young egg chamber maintenance under nutrient starvation. Here, we show that knockdown of RagA results in young egg chamber death independent of TORC1 hyperactivity. RagA RNAi ovaries have autolysosomal acidification and degradation defects, which make the young egg chambers sensitive to autophagosome augmentation. Meanwhile, RagA RNAi ovaries have nuclear-localized Mitf, which promotes autophagic degradation and protects young egg chambers under stress. Interestingly, GDP-bound RagA rescues autolysosome defects, while GTP-bound RagA rescues Mitf nuclear localization in RagA RNAi young egg chambers. Moreover, Rag GTPase activity, rather than TORC1 activity, controls Mitf cellular localization in the Drosophila germ line. Our work suggests that RagA separately controls autolysosomal acidification and Mitf activity in the Drosophila young egg chambers.

[The regulatory relationship between RagA and Nprl2 in Drosophila gut development].

The gastrointestinal tract is the largest digestive organ and the largest immune organ and detoxification organ, which is vital to the health of the body. Drosophila is a classic model organism, and its gut is highly similar to mammalian gut in terms of cell composition and genetic regulation, therefore can be used as a good model for studying gut development. target of rapmaycin complex 1 (TORC1) is a key factor regulating cellular metabolism. Nprl2 inhibits TORC1 activity by reducing Rag GTPase activity. Previous studies have found that nprl2 mutated Drosophila showed aging-related phenotypes such as enlarged foregastric and reduced lifespan, which were caused by over-activation of TORC1. In order to explore the role of Rag GTPase in the developmental defects of the gut of nprl2 mutated Drosophila, we used genetic hybridization combined with immunofluorescence to study the intestinal morphology and intestinal cell composition of RagA knockdown and nprl2 mutated Drosophila. The results showed that RagA knockdown alone could induce intestinal thickening and forestomach enlargement, suggesting that RagA also plays an important role in intestinal development. Knockdown of RagA rescued the phenotype of intestinal thinning and decreased secretory cells in nprl2 mutants, suggesting that Nprl2 may regulate the differentiation and morphology of intestinal cells by acting on RagA. Knockdown of RagA did not rescue the enlarged forestomach phenotype in nprl2 mutants, suggesting that Nprl2 may regulate forestomach development and intestinal digestive function through a mechanism independent of Rag GTPase.