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This paper's research objective is to investigate an independent ship with wind-solar-diesel-battery hybrid energy using real-time variations of energy source components in energy storage systems. The costs of fuel, and sewage and real-time output cost of a diesel generator set and energy storage system are also considered. Firstly, this paper investigates the critical output point of energy storage systems under a dynamic load, to determine the priority of energy storage control strategy. Secondly, this paper investigates the issue of power supply optimisation. A three objective optimisation design model is proposed, which includes the cost of the whole life cycle of the system, the microgrid capacity loss and the pollutant treatment cost. This paper also uses the NSGA-II algorithm which is used to investigate the numerous aspects of independent ship microgrid optimisation, while influencing different power combinations and energy control strategies. The results show that the method is accurate and effective.

To study the performance of partial air cushion-supported catamaran (PACSCAT), which is sailing with a flexible air seal in waves, this paper uses the model tests, and research the motion characteristics of PACSCAT at different wavelengths, by monitoring the boundaries of heave, pitch, acceleration, air cushion pressure. Firstly this paper introduces the test situation of PACSCAT in the towing tank and introduces the test method, equipment, and test conditions. Second, this paper extracts the test data, analyzes the features of heave, pitch, acceleration, and air cushion pressure, and studies their linear and nonlinear changes in regular waves. Thirdly this paper analyzes the nonlinear air leakage flow of the bow of PACSCAT in detail under the test conditions and studies the internal and external free liquid surface under different conditions.

Depletion of glutathione (GSH) from CYP2E1-expressing cells by treatment with l-buthionine sulfoximine (BSO) causes decreased cell viability. The possible role of mitogen-activated protein kinases (MAPK) in this toxicity was evaluated. SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole], an inhibitor of p38 MAPK decreased the BSO-dependent toxicity in HepG2 E47 cells, which express CYP2E1 and in hepatocytes from pyrazole-treated rats. Inhibitors of extracellular signal-regulated kinase, phosphatidylinositol 3-kinase, and c-Jun amino-terminal kinase were not protective. SB203580 did not prevent the loss of GSH nor lower the increase in reactive oxygen production; hence, protection by SB203580 was downstream of the elevated oxidative stress. Treatment with BSO caused activation of p38 MAPK whereas activation of nuclear factor-kappaB (NF-kappaB) was decreased; these effects were prevented by SB203580. We speculated that the decrease in NF-kappaB activation prevented production of hepatoprotective factors. One such factor could be nitric oxide (NO); indeed a NO donor decreased the BSO plus CYP2E1-dependent toxicity, whereas inhibition of inducible NO synthase (iNOS) potentiated toxicity. BSO treatment down-regulated iNOS and lowered NO levels, reactions blocked by SB203580; however, protection by SB203580 was the same in the absence or presence of an iNOS inhibitor, indicating that recovery of iNOS and NO production was not the mechanism by which SB203580 afforded protection against the BSO plus CYP2E1-dependent toxicity. Presumably other protective factors besides nitric oxide may be produced from activated NF-kappaB when p38 MAPK is inhibited by SB203580. These results suggest that the activation of p38 MAPK by BSO treatment in CYP2E1-expressing liver cells cause a loss in NF-kappaB-dependent production of hepatoprotective factors. This loss, coupled to CYP2E1-generated oxidant stress, synergize to promote cell injury.