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Due to their extreme requirements, conventional Ni–Ti shape memory alloys (SMAs) are no longer suitable for aerospace applications. Adding Hf to Ni–Ti SMAs can significantly enhance their suitability for aerospace applications, particularly in high-temperature environments. In this regard, the hot/thermal deformation behavior of Ni50.4Ti34.6Hf15 high-temperature shape memory alloys (HTSMAs) was systematically investigated by using a Gleeble-3800 thermocompression simulation machine. The results prove that the Ni50.4Ti34.6Hf15 alloys have more strain sensitivity than the temperature during the hot/thermal deformation process. In detail, the flow stress increases with the increase in strain rate and decreases with the increase in deformation temperature. From the microstructure evolution point of view, the recovery effect will increase with the increase in deformation temperature, and the recrystallization effect will increase with the increase in strain rate. Following the obtained stress-strain curves, the flow behavior of Ni50.4Ti34.6Hf15 alloys during hot/thermal deformation was established. A modified constitutive equations model was proposed using careful consideration of deformation temperature and strain rate. It was found that the calculated strain activation energy was 363.945 kJ/mol in the range of 700∼800 °C and 512.489 kJ/mol in the range of 900∼1000 °C. Based on the constitutive equation, the calculated values were consistent with the experimental values, which indicated reliable analysis with high prediction accuracy. Furthermore, the thermal processing maps under different conditions were constructed, and it was determined that the optimum hot/thermal deformation processing parameters of Ni50.4Ti34.6Hf15 alloys were 940∼1000 °C and 0.01–0.04 s−1.

Exercise benefits the whole organism, yet, how tissues across the body orchestrally respond to exercise remains enigmatic. Here, in young and old mice, with or without exercise, and exposed to infectious injury, we characterized the phenotypic and molecular adaptations to a 12-month exercise across 14 tissues/organs at single-cell resolution. Overall, exercise protects tissues from infectious injury, although more effectively in young animals, and benefits aged individuals in terms of inflammaging suppression and tissue rejuvenation, with structural improvement in the central nervous system and systemic vasculature being the most prominent. In vascular endothelial cells, we found that readjusting the rhythmic machinery via the core circadian clock protein BMAL1 delayed senescence and facilitated recovery from infectious damage, recapitulating the beneficial effects of exercise. Our study underscores the effect of exercise in reconstituting the youthful circadian clock network and provides a foundation for further investigating the interplay between exercise, aging, and immune challenges across the whole organism.