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This paper presents a numerical simulation of the geometry and the pressure distribution of a ventilated supercavity at different cavitator amplitudes and periods of motion. The numerical method is validated by comparing with the results of a semi-empirical formula under specific conditions. It is shown that the simulation can capture the boundary fluctuations of the ventilated supercavity and its internal pressure variations in a cavitator motion cycle. The simulation results show that the supercavity boundary experiences wave-like deformations when the wavelength of the disturbance caused by the cavitator motion is comparable to the supercavity length. It is also shown that the supercavity closure changes in form between a re-entrant jet and a twin vortex owing to the variations of the pressure difference between the outside and the inside of the supercavity near the closure region. The maximum diameter of the ventilated supercavity exhibits periodic changes with a double peak in each cavitator motion cycle, caused by the corresponding changes of the difference between the internal and external pressures. With the increase of the amplitude of motion of the cavitator, the supercavity boundary has enhanced wave-like undulations, with an increased maximum diameter, and with fluctuations in the cavitation number. As the period of the cavitator motion increases, the wavelength of the disturbances caused by this motion becomes greater than the supercavity length, and so the wave-like undulations of the supercavity boundary and the maximum diameter of the supercavity gradually decrease, but the variations of the cavitation number increase. Moreover, with the increase of the periods, the delay effects on the variations of the characteristics of the supercavity geometry caused by cavitator motion gradually decrease, and they practically vanish for large periods. [ABSTRACT FROM AUTHOR]

This paper studies the gas-liquid flow splitting in T-junction with inclined lateral arm. The separation mechanism of the T-junction is related to the pressure distribution in the T-junction. It is shown that the separation efficiency strongly depends on the inclination angle, when the angle ranges from 0° to 30°, while not so strongly for angles in the range from 30° to 90° Increasing the number of connecting tubes is helpful for the gas-liquid separation, and under the present test conditions, with four connecting tubes, a good separation performance can be achieved. Accordingly, a multi-tube Y-junction separator with four connecting tubes is designed for the experimental investigation. A good agreement between the simulated and measured data shows that there is an optimal split ratio to achieve the best performance for the multi-tube Y-junction separator. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Ginsenosides regulate glucose homeostasis. This study investigated the effect of ginsenoside Rg5 (Rg5) on the hepatic glucagon response, focusing on the regulation of metabolism. Methods: Mice fed a high-fat diet (HFD) showed increased hepatic glucose production (HGP). We observed the effects of Rg5 on hepatic fatty acid oxidation and glucagon response. The regulation of phosphodiesterase (PDE) 4B by succinate was also investigated in hepatocytes. Results: Rg5 inhibited endogenous glucose production in HFD-fed mice. Rg5 reduced cyclic AMP (cAMP) accumulation and inhibited transcriptional regulation of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) by dephosphorylation of the cAMP response element-binding transcription factor in the liver, demonstrating the inhibitory effect on hepatic glucagon response. HFD feeding increased succinate accumulation in the liver due to the reversal of succinate dehydrogenase activation and triggered hypoxia-inducible factor-1α (HIF-1α) induction. Succinate prevented cAMP degradation by inactivating PDE4B, thereby increasing cAMP accumulation in response to glucagon. Knockdown of HIF-1α with small interfering RNA diminished the effect of succinate, indicating that HIF-1α was essential for succinate to inactivate PDE4B. Rg5 inhibited succinate accumulation in hepatocytes by combating fatty acid oxidation, and thus reduced cAMP accumulation by blocking succinate/HIF-1α induction. Rg5 reduced HGP as a consequence of the inhibition of the glucagon response. Conclusions/interpretation: Succinate acted as a metabolic signal to enhance the hepatic glucagon response. Rg5 reduced hepatic succinate accumulation by combating fatty acid oxidation and attenuated the hepatic glucagon response by suppressing succinate/HIF-1α induction, suggesting that succinate-associated HIF-1α induction in hepatocytes might be a therapeutic target in the treatment of diabetes. [ABSTRACT FROM AUTHOR]