ABSTRACT
Expansive soil exhibits remarkable characteristics of water absorption expansion and water loss shrinkage, rendering it susceptible to cracking under the alternating dry-wet environments of nature. The generation and development of cracks in expansive soil can result in catastrophic engineering accidents such as landslides. Vegetation protection is an important approach to stabilizing expansive soil slopes and fulfilling ecological protection requirements. In this study, through indoor experiments and theoretical analysis methods, the effects of Cynodon dactylon roots on the crack development and shear strength of expansive soil subjected to dry-wet cycles were analyzed, and the relationship between the crack development and shear strength decay in root-doped expansive soil was explored. Furthermore, the mechanism of vegetative root system action was elucidated. The results show that the Cynodon dactylon root system exerts a significant inhibitory effect on crack development in expansive soil. The crack indexes of root-doped expansive soil exhibit significant phase characteristics during the process of dry-wet cycles. The crack-blocking and reinforcing effect of the root system becomes pronounced as the root-to-soil mass ratio increases and the root diameter decreased. Moreover, the process of crack development in expansive soil is accompanied by a decrease in soil shear strength. The quantitative relationship between crack development and shear strength decay can serve as a basis for predicting the stability of slope soil. Overall, the results highlight the potential of vegetation-based approaches in protecting slopes with expansive soils and have practical implications for ecological protection and engineering design in areas with expansive soils.
Subject(s)
Cynodon , Soil , Shear Strength , WaterABSTRACT
Background: Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder leading to cognitive impairment in the elderly, and no effective treatment exists. Increasing evidence has demonstrated that physical therapy and electroacupuncture (EA) effectively improve spatial learning and memory abilities. Nevertheless, the mechanism underlying the effects of EA on AD pathology is largely unexplored. Acupuncture at Zusanli (ST 36) has previously been shown to improve cognitive impairment in AD, but the mechanism is unclear. According to recent studies, EA drives the vagal-adrenal axis from the hindlimb ST 36 acupoint but not from the abdominal Tianshu (ST 25) to curb severe inflammation in mice. This study examined whether ST 36 acupuncture improves cognitive dysfunction in AD model mice by improving neuroinflammation and its underlying mechanism. Methods: Male 5xFAD mice (aged 3, 6, and 9 months) were used as the AD animal model and were randomly divided into three groups: the AD model group (AD group), the electroacupuncture at ST 36 acupoint group (EA-ST 36 group), and the electroacupuncture at ST 25 acupoint group (EA-ST 25 group). Age-matched wild-type mice were used as the normal control (WT) group. EA (10 Hz, 0.5 mA) was applied to the acupoints on both sides for 15 min, 5 times per week for 4 weeks. Motor ability and cognitive ability were assessed by the open field test, the novel object recognition task, and the Morris water maze test. Thioflavin S staining and immunofluorescence were used to mark Aß plaques and microglia. The levels of NLRP3, caspase-1, ASC, interleukin (IL)-1ß, and IL-18 in the hippocampus were assayed by Western blotting or qRT-PCR. Results: EA at ST 36, but not ST 25, significantly improved motor function and cognitive ability and reduced both Aß deposition and microglia and NLRP3 inflammasome activation in 5×FAD mice. Conclusion: EA stimulation at ST 36 effectively improved memory impairment in 5×FAD mice by a mechanism that regulated microglia activation and alleviated neuroinflammation by inhibiting the NLRP3 inflammatory response in the hippocampus. This study shows that ST 36 may be a specific acupoint to improve the condition of AD patients.