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In the realm of van design, researchers have been diligently working to enhance rollover crashworthiness while concurrently achieving lightweight body structures. Unlike front and side impacts, rollover crashworthiness is impacted by a greater number of structural dimensions and material parameters. As such, this paper implements an unreplicated saturated factorial design to conduct factor screening for vehicle rollover crashworthiness. This approach effectively and accurately resolves the screening challenges that arise from large numbers of factors, and eliminates dependence on traditional design experience. Consequently, it shortens the design cycle and reduces development costs. In addition, this paper establishes four Kriging approximate models that describe the specific energy absorption and total mass of the key body structure, the displacement of the roof, and the maximum angular velocity of the body's center of mass. To address the multi-objective optimization problem of improving rollover crashworthiness while reducing mass, this paper combines the particle swarm optimization algorithm with the artificial immune algorithm. This hybrid algorithm converges rapidly, and the Pareto solution set exhibits superior uniformity and diversity. Finally, the shortest distance method is employed to identify the optimal design scheme that can enhance the rollover crashworthiness of vans and reduce the mass of body parts. [ABSTRACT FROM AUTHOR]

Objective: Smooth muscle cell (SMC) phenotypic switching is associated with development of a variety of occlusive vascular diseases. Paeonol has been reported to be involved in suppressing SMC proliferation. However, it is still unknown whether paeonol can regulate SMC phenotypic switching, and which eventually result in suppressing vasculogenesis. Methods: Murine left common carotid artery was injured by completely ligation, and paeonol was administrated by intraperitoneal injection. Hematoxylin and eosin (H&E) staining was performed to visualize vascular neointima formation. Rat aortic SMCs were used to determine whether paeonol suppresses cell proliferation and migration. And murine hind limb ischemia model was performed to confirm the function role of paeonol in suppressing vasculogenesis. Results: Complete ligation of murine common carotid artery successfully induced neointima formation. Paeonol treatment dramatically reduced the size of injury-induced neointima. Using rat aortic primary SMC, we identified that paeonol strongly suppressed cell proliferation, migration, and decreased extracellular matrix deposition. And paeonol treatment dramatically suppressed vasculogenesis after hind limb ischemia injury. Conclusion: Paeonol could regulate SMC phenotypic switching through inhibiting proliferation and migration of SMC, which results in inhibiting ischemia-induced vasculogenesis. [ABSTRACT FROM AUTHOR]