A vertical spring-viscous damper-concave Coulomb friction isolation system was firstly proposed, and their parameters were firstly optimized to achieve the best performance under earthquakes. An incremental dynamic analysis method (IDA) and a performance-based assessment framework were used to calculate the system and assess its seismic vulnerability, respectively. Results show that both the friction force and the horizontal component of spring force gradually increase when an earthquake enforce the isolator to slide from its central location. Although other papers propose that an increase of spring force and a decrease of friction force can reduce the structural residual displacement, this paper can minimize the residual displacement value to be 0 by using a super lubrication in the middle of contact surface and a variable increment ratio of concave friction distribution. The reason is that the horizontal component of spring force is always greater than the friction force within any relative displacement between the structure and the ground in this paper. As for the peak relative displacement and peak acceleration of structure, one is reduced while the other is increased when selecting the optimal isolation parameters. If the structure is very sensitive to the acceleration response, a low friction parameter, a small spring constant, and a small and even zero damping constant could be adopted to yield a small peak acceleration of system. The tightness of vertical spring can be adjusted to be appropriately loose to continuously reduce the structural acceleration response.

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Objective: Recently, the protective effect of exosomes on ischemia/reperfusion (I/R) injury has become a research hotspot. The purpose of this study was to explore the therapeutic potential of microglia-derived exosomes on cerebral I/R injury. Methods: BV2 cell-derived exosomes (BV2-Exo) were extracted and characterized. The cerebral I/R model was constructed in vivo and intervened by using exosomes loaded with miR-302a-3p. The oxygen and glucose deprivation (OGD) model was constructed in vitro to simulate cerebral I/R injury. The binding sites of miR-302a-3p to Keap1 were analyzed by bioinformatics prediction and confirmed by dual-luciferase reporter assay. A study of whether exosomal miR-302a-3p affected cerebral I/R injury via the Keap1/Nrf2 axis was carried out by overexpression of keap1 (oe-keap1). Results: Experimental results in vivo showed exosomal miR-302a-3p significantly repaired the cognitive impairment and suppressed the apoptosis of hippocampal neurons induced by cerebral I/R injury. Besides, exosomal miR-302a-3p inhibited the expression of ferroptosis-related proteins NCOA4, PTGS2, and p53 in cerebral I/R-treated mice. Bioinformatics prediction and double-luciferase reporter assay showed that Keap1 was the direct downstream target of miR-302a-3p. Experiment results in vitro showed that oe-Keap1 reversed the therapeutic effect of exosomal miR-302a-3p on cerebral I/R injury via the Keap1/Nrf2 axis, promoting the high expression of NCOA4, PTGS2, and p53 and the increase of Fe2+, MDA and ROS levels. Conclusion: The results demonstrated that microglia-exosomal miR-302a-3p suppressed ferroptosis to alleviate cerebral I/R injury by inhibiting neuronal ferritinophagy via regulating the Keap1/Nrf2 axis.

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