Double-clamped bistable buckled beams, as the most elegant bistable mechanisms, demonstrate great versatility in various fields, such as robotics, energy harvesting, and MEMS. However, their design is always hindered by time-consuming and expensive computations. In this work, we present a method to easily and rapidly design bistable buckled beams subjected to a transverse point force. Based on the Euler-Bernoulli beam theory, we establish a theoretical model of bistable buckled beams to characterize their snap-through properties. This model is verified against the results from an FEA model, with discrepancy less than 7%. By analyzing and simplifying our theoretical model, we derive explicit analytical expressions for critical behavioral values on the force-displacement curve of the beam. These behavioral values include critical force, critical displacement, and travel, which are generally sufficient for characterizing the snap-through properties of a bistable buckled beam. Based on these analytical formulas, we investigate the influence of a bistable buckled beam's key design parameters, including its actuation position and precompression, on its critical behavioral values, with our results validated by FEA simulations. This way, our method enables fast and computationally inexpensive design of bistable buckled beams and can guide the design of complex systems that incorporate bistable mechanisms.
DL-3-n-butylphthalide (NBP) is commonly used to treat ischemic strokes due to its antioxidative and anti-inflammatory effects. The present study aimed to examine the protective effects of NBP on myocardial ischemia-reperfusion injury (MIRI) by establishing a MIRI model in H9c2 cells. Cell viability assay using Cell Counting Kit-8, lactate dehydrogenase (LDH) cytotoxicity and lipid peroxidation malondialdehyde (MDA) content were assessed to detect cell activity, degree of cell injury and oxidative stress reaction. Reverse transcription-quantitative PCR was used to quantify the expression of inflammatory factors in H9c2 cells. Western blotting and immunofluorescence staining were used to detect the protein expression of PI3K/AKT and heat shock protein 70 (HSP70). The present results indicated that NBP significantly increased cell viability during ischemia-reperfusion. Moreover, NBP inhibited the release of LDH and the production of MDA. NBP treatment also significantly decreased the expression of inflammatory factors at the mRNA level. Additionally, NBP activated the PI3K/AKT pathway and upregulated the expression of HSP70 compared with cells in the MIRI model. LY294002, a PI3K inhibitor, reversed the protective effects of NBP and suppressed the expression of HSP70. The present study demonstrated that NBP protected H9c2 cells from MIRI by regulating HSP70 expression via PI3K/AKT pathway activation.
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