EV battery charging is growing in importance as it has a direct influence on the EV performance. Multistage Constant Current (MCC) charging strategy is an effective rapid charging method. This paper proposes an ECM-PSO algorithm to search for the optimal current pattern of the MCC charging strategy. The MCC charging model is built according to the Li-ion battery equivalent circuit model, and the object function for the ECM-PSO optimization was formulated and the optimal current pattern of the MCC charging method was obtained through the ECM-PSO algorithm. The experimental result shows that the obtained current pattern is capable of charging the batteries to 87.7% of the rated capacity within 36.5 min. Compared with the conventional CC-CV charging method, the proposed charging strategy has a performance improvement of 60.3% in charging time reduction, and the average temperature rise during the proposed MCC charging process is 0.5 ℃ lower than the CC-CV charging method.

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The essential yeast kinases Mec1 and Rad53, or human ATR and Chk1, are crucial for checkpoint responses to exogenous genotoxic agents, but why they are also required for DNA replication in unperturbed cells remains poorly understood. Here we report that even in the absence of DNA-damaging agents, the rad53-4AQ mutant, lacking the N-terminal Mec1 phosphorylation site cluster, is synthetic lethal with a deletion of the RAD9 DNA damage checkpoint adaptor. This phenotype is caused by an inability of rad53-4AQ to activate the downstream kinase Dun1, which then leads to reduced basal deoxynucleoside triphosphate (dNTP) levels, spontaneous replication fork stalling, and constitutive activation of and dependence on S phase DNA damage checkpoints. Surprisingly, the kinase-deficient rad53-K227A mutant does not share these phenotypes but is rendered inviable by additional phosphosite mutations that prevent its binding to Dun1. The results demonstrate that ultralow Rad53 catalytic activity is sufficient for normal replication of undamaged chromosomes as long as it is targeted toward activation of the effector kinase Dun1. Our findings indicate that the essential S phase function of Rad53 is comprised by the combination of its role in regulating basal dNTP levels and its compensatory kinase function if dNTP levels are perturbed.

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