shock wave
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AbstractMitigation of pressure pulsations in the exhaust of a pulse detonation combustor is crucial for operation with a downstream turbine. For this purpose, a device termed the shock divider is designed and investigated. The intention of the divider is to split the leading shock wave into two weaker waves that propagate along separated ducts with different cross sections, allowing the shock waves to travel with different velocities along different paths. The separated shock waves redistribute the energy of the incident shock wave. The shock dynamics inside the divider are investigated using numerical simulations. A second-order dimensional split finite volume MUSCL-scheme is used to solve the compressible Euler equations. Furthermore, low-cost simulations are performed using geometrical shock dynamics to predict the shock wave propagation inside the divider. The numerical simulations are compared to high-speed schlieren images and time-resolved total pressure recording. For the latter, a high-frequency pressure probe is placed at the divider outlet, which is shown to resolve the transient total pressure during the shock passage. Moreover, the separation of the shock waves is investigated and found to grow as the divider duct width ratio increases. The numerical and experimental results allow for a better understanding of the dynamic evolution of the flow inside the divider and inform its capability to reduce the pressure pulsations at the exhaust of the pulse detonation combustor.

Abstract In previous studies, we found radial extracorporeal shock wave (rESW), can promote the proliferation of neural stem cells（NSCs）. Emerging evidence suggests that lncRNA NEAT1 can regulate NSCs proliferation. Whether lncRNA NEAT1 plays a role in the proliferation of NSC induced by shock waves is unclear. Cell Counting Kit-8（CCK 8） method was used to detect the proliferation of NSCs, and the relative protein and mRNA expression of related genes of Nestin, Cyclin D1 and P21 were detected by Western Blot and Quantitative real-time PCR（RT-qPCR）respectively. Immunofluorescence staining was used to observe the changes in the number of BrdU/nestin positive cells. Overexpression of NEAT1 and let 7b in cells were used to explore whether rESW can rescue the decreased number of NSCs.We found that the optimal dose of R15 transmitter promoting NSCs proliferation is 1.5 bar, 500 pulse, 2 Hz. 1.2-1.5bar showed a dose-dependent effect on the proliferation of NSCs, but it was negatively correlated with the proliferation effect of NSC when it was more than 1.5bar. We revealed that let 7b-P21 axis was involved in regulating the inhibition of NSC proliferation which was activated by NEAT1 in NSCs. In addition, we demonstrated that rESW treatment resulted in the decrease of NEAT1 expression, which was accompanied by the improved biological function including proliferation.Our results confirm that low-intensity rESW（1.5bar，500pulse，2Hz） can promote the proliferation of NSCs through NEAT1-let 7b-P21 axis.

Experimental studies of the influence of fluid–structure interaction on cloud cavitation about a stiff stainless steel (SS) and a flexible composite (CF) hydrofoil have been presented in Parts I (Smith et al., J. Fluid Mech., vol. 896, 2020a, p. A1) and II (Smith et al., J. Fluid Mech., vol. 897, 2020b, p. A28). This work further analyses the data and complements the measurements with reduced-order model predictions to explain the complex response. A two degrees-of-freedom steady-state model is used to explain why the tip bending and twisting deformations are much higher for the CF hydrofoil, while the hydrodynamic load coefficients are very similar. A one degree-of-freedom dynamic model, which considers the spanwise bending deflection only, is used to capture the dynamic response of both hydrofoils. Peaks in the frequency response spectrum are observed at the re-entrant jet-driven and shock-wave-driven cavity shedding frequencies, system bending frequency and heterodyne frequencies caused by the mixing of the two cavity shedding frequencies. The predictions capture the increase of the mean system bending frequency and wider bandwidth of frequency modulation with decreasing cavitation number. The results show that, in general, the amplitude of the deformation fluctuation is higher, but the amplitude of the load fluctuation is lower for the CF hydrofoil compared with the SS hydrofoil. Significant dynamic load amplification is observed at subharmonic lock-in when the shock-wave-driven cavity shedding frequency matches with the nearest subharmonic of the system bending frequency of the CF hydrofoil. Both measurements and predictions show an absence of dynamic load amplification at primary lock-in because of the low intensity of cavity load fluctuations with high cavitation number.

Background: Stem cell-derived exosomes have great potential in the treatment of myocardial ischemia–reperfusion injury (IRI). Extracorporeal cardiac shock waves (ECSW) as effective therapy, in part, could activate the function of exosomes. In this study, we explored the effect of ECSW-induced exosome derived from endothelial colony-forming cells on cardiomyocyte hypoxia/reoxygenation (H/R) injury and its underlying mechanisms.Methods: The exosomes were extracted and purified from the supernatant of endothelial colony-forming cells (ECFCs-exo). ECFCs-exo treated with shock wave (SW-exo) or without shock wave (CON-exo) were performed with high-throughput sequencing of the miRNA. H9c2 cells were incubated with SW-exo or CON-exo after H/R injury. The cell viability, cell apoptosis, oxidative stress level, and inflammatory factor were assessed. qRT-PCR was used to detect the expression levels of miRNA and mRNA in cells and exosomes. The PTEN/PI3K/AKT pathway-related proteins were detected by Western blotting, respectively.Results: Exosomes secreted by ECFCs could be taken up by H9c2 cells. Administration of SW-exo to H9c2 cells after H/R injury could significantly improve cell viability, inhibit cell apoptosis, and downregulate oxidative stress level (p < 0.01), with an increase in Bcl-2 protein and a decrease in Bax, cleaved caspase-3, and NF-κB protein (p < 0.05). Notably, miR-140-3p was found to be highly enriched both in ECFCs and ECFCs-exo treated with ECSW (p < 0.05) and served as a critical mediator. SW-exo increased miR-140-3p expression but decreased PTEN expression in H9c2 cells with enhanced phosphorylation of the PI3K/AKT signaling pathway. These cardioprotective effects of SW-exo on H/R injury were blunted by the miR-140-3p inhibitor. Dual-luciferase assay verified that miR-140-3p could directly target the 3′UTR of PTEN mRNA and exert a negative regulatory effect.Conclusion: This study has shown the potential of ECSW as an effective stimulation for the exosomes derived from ECFCs in vitro. SW-exo exerted a stronger therapeutic effect on H/R injury in H9c2 cells possibly via delivering exosomal miR-140-3p, which might be a novel promising strategy for the myocardial IRI.