In order to investigate the vibration characteristics of a composite sleeper-ballasted track and provide a basis for further popularization, a vehicle–track dynamic coupling model is established and the viscoelastic properties of the composite sleeper are considered. The power flow method is employed to reveal the power flow distribution characteristics of the composite sleeper. The results show that the viscoelastic properties of the composite sleeper have little influence on the rail power and have a greater influence on the power flow of the sleeper and ballast bed in some frequency ranges. The viscoelastic properties of the composite sleeper can effectively improve the calculation accuracy of the track structure’s power flow. Compared with the type-III pre-stressed concrete sleepers widely used in China, composite sleepers consume more energy in the vibration process due to their own physical characteristics, which reduces the power flow transmitted downward and relieves vibration on the ballast bed, especially in the ranges of 80–125 Hz and 250–400 Hz. The temperature change mainly affects the power flow of the composite sleeper in the frequency range above 50 Hz. As the temperature increases, the modulus of the composite sleeper decreases and the vibration reduction effect of the ballast bed is improved.
In order to study the vertical dynamic characteristics of the composite sleeper ballasted track in tunnels, this paper establishes a dynamic model based on the finite element method, and compares the dynamic response of vehicle, wheel and rail systems, track systems and backfill layer with the type-III concrete sleeper. The research results show that the composite sleeper ballasted tracks’ acceleration of the car body and the wheel-rail force are smaller than that of the type-III sleeper. It can meet the safety of the train and passenger comfort. Because the composite sleeper has good elasticity, The rail displacement and acceleration, the sleeper displacement and acceleration of the composite sleeper are slightly larger than the type-III sleeper ballasted track, but the effect is not great. The composite sleeper has good elasticity and large damping, so that the acceleration of the track bed and the backfill layer is less than that of the type-III sleeper ballasted track. This shows that the composite sleeper has vibration damping characteristics for the track bed and the backfill layer.
Our previous studies have demonstrated that mitochondrial membrane potential ( ΔΨ m ) dissipation leads to mitochondrial Ca efflux via the mitochondrial permeability transition pore (mPTP), and consequently promotes spontaneous Ca waves (CaW) in isolated cardiomyocytes. In the present study, we have used a genetic mouse model which lacks cyclophilin D (CypD KO), a necessary regulator for mPTP opening, to assess the cardioprotective effect of mPTP inhibition on cellular CaWs, Ca alternans, and whole-heart inducible arrhythmias. Ventricular myocytes were isolated from wild type (WT) and CypD KO mice. Tetramethylrhodamine (TMRM) was used as an indicator of ΔΨ m. Mitochondrial calcein release was used as the index of mPTP opening. Cytosolic Ca was imaged using Fluo-4-AM. Spontaneous CaWs were induced in the presence of 4mM external Ca. The protonophore FCCP was used to depolarize Δ Ψ m . FCCP caused Δ Ψ m depolarization to the same extent in both WT and CypD KO myocytes, however, CypD KO cells exhibited significantly less mPTP opening than WT cells (p < 0.05). Consistent with these results, treatment with FCCP caused significant increases in WT CaW rate but no increase in CypD KO CaW rate. These results were further confirmed by treating WT cells with the mPTP blocker cyclosporin A (CsA). Furthermore, occurrence of Ca alternans after treatment with FCCP and programmed stimulation was observed in a significantly higher number of WT cells (11 of 13), than in WT cells treated with CsA (2 of 8; p < 0.05) or CypD KO cells (2 of 10; p < 0.01). At the whole-heart level, pseudo-Lead II ECGs were recorded from ex vivo, Langendorff-perfused WT and CypD KO hearts, and the incidences of T-wave alternans (a precursor of lethal arrhythimas) and arrhythmias induced by programmed S 1 -S 2 stimulation were compared. We observed T-wave alternans in 5 of 7 WT hearts, but none in 5 CypD KO hearts (p < 0.05) and in only 1 of 6 WT hearts treated with CsA (p <0.05). Consistent with these results, WT hearts exhibited a significantly higher average arrhythmia score than CypD KO (p <0.01) or WT hearts treated with CsA (p < 0.01). In conclusion, CypD deficiency-induced mPTP inhibition attenuates CaWs and Ca alternans during mitochondrial depolarization, and thereby protects against arrhythmogenesis in the heart.
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