Study on the formation of arc plasma on the resistive wall liquid metal current limiter

Due to its significant attributes,the liquid metal current limiter(LMCL)is considered a new strategy for limiting short-circuit current in the power grid.A resistive wall liquid metal current limiter(RWLMCL)is designed to advance the starting current-limiting time.Experiments are performed to investigate the dynamic behaviors of liquid metal,and the influence of different currents on the liquid metal self-shrinkage effect is compared and analyzed.Furthermore,the liquid metal self-shrinkage effect is mathematically modeled,and the reason for the formation of arc plasma is obtained by simulation.The laws of arc plasma formation and the current transfer in the cavity are revealed,and the motion mechanisms are explained by physical principles.The simulations are in accordance with the test data.It is demonstrated that the sudden change of the current density at both ends of the wall causes the liquid metal to shrink and depress under the electromagnetic force,and the current starts to transfer from the liquid metal path to the wall resistance path.The RWLMCL can effectively advance the starting current-limiting time.

A novel fault current limiter topology design based on liquid metal current limiter

The liquid metal current limiter(LMCL)is regarded as a viable solution for reducing the fault current in a power grid.But demonstrating the liquid metal arc plasma self-pinching process of the resistive wall,and reducing the erosion of the LMCL are challenging,not only theoretically,but also practically.In this work,a novel LMCL is designed with a resistive wall that can be connected to the current-limiting circuit inside the cavity.Specifically,a novel fault current limiter(FCL)topology is put forward where the novel LMCL is combined with a fast switch and current-limiting reactor.Further,the liquid metal self-pinch effect is modeled mathematically in three dimensions,and the gas-liquid two-phase dynamic diagrams under different short-circuit currents are obtained by simulation.The simulation results indicate that with the increase of current,the time for the liquid metal-free surface to begin depressing is reduced,and the position of the depression also changes.Different kinds of bubbles formed by the depressions gradually extend,squeeze,and break.With the increase of current,the liquid metal takes less time to break,but breaks still occur at the edge of the channel,forming arc plasma.Finally,relevant experiments are conducted for the novel FCL topology.The arcing process and current transfer process are analyzed in particular.Comparisons of the peak arc voltage,arcing time,current limiting efficiency,and electrode erosion are presented.The results demonstrate that the arc voltage of the novel FCL topology is reduced by more than 4.5times and the arcing time is reduced by more than 12%.The erosions of the liquid metal and electrodes are reduced.Moreover,the current limiting efficiency of the novel FCL topology is improved by 1%–5%.This work lays a foundation for the topology and optimal design of the LMCL.

CD4 T cell deficiency attenuates ischemic stroke, inhibits oxidative stress, and enhances Akt/mTOR survival signaling pathways in mice

Background: Inhibition of CD4 T cells reduces stroke-induced infarction by inhibiting neuroinflammation in the ischemic brain in experimental stroke. Nevertheless, little is known about its effects on neuronal survival signaling pathways. In this study, we investigated the effects of CD4 T cell deficits on oxidative stress and on the Akt/mTOR cell signaling pathways after ischemic stroke in mice. Methods: MHC II gene knockout C57/BL6 mice, with significantly decreased CD4 T cells, were used. Stroke was induced by 60-min middle cerebral artery (MCA) occlusion. Ischemic brain tissues were harvested for Western blotting. Results: The impairment of CD4 T cell production resulted in smaller infarction. The Western blot results showed that iNOS protein levels robustly increased at 5 h and 24 h and then returned toward baseline at 48 h in wild-type mice after stroke, and gene KO inhibited iNOS at 5 h and 24 h. In contrast, the anti-inflammatory marker, arginase I, was found increased after stroke in WT mice, which was further enhanced in the KO mice. In addition, stroke resulted in increased phosphorylated PTEN, Akt, PRAS40, P70S6, and S6 protein levels in WT mice, which were further enhanced in the animals whose CD4 T cells were impaired. Conclusion: The impairment of CD4 T cell products prevents ischemic brain injury, inhibits inflammatory signals, and enhances the Akt/mTOR cell survival signaling pathways.