In fuel cell vehicles, the output voltage of the fuel cell source is typically much lower than the voltage required by the DC bus and also this output voltage drops significantly as the output current increases. In order to match the output voltage of the fuel cell source to the DC bus voltage, a new DC-DC boost converter with a wide input range and high voltage gain is proposed to act as the required power interface, which reduces voltage stress across the power devices and operates with an acceptable conversion efficiency. A prototype rated at 300W/400V has been developed and the maximum efficiency of the proposed converter was measured as 95.01% at 300W. Experimental results are presented to validate the effectiveness of the proposed converter.Index Terms-Boost DC-DC converter, Fuel cell Vehicles, High voltage-gain, Switched-capacitor, Wide input range.

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Spinal cord injury (SCI) leads to the loss of structure and function of axons. However, injured axons cannot grow or regenerate spontaneously following injury. Generally, only when treated with neurotrophins, such as nerve growth factor (NGF), will the neurons sprout new axons. Akt is one of the central kinases of neurocytes. PC12 cells are a frequently used cell model for neural differentiation and development studies. The nuclear factor erythroid 2‑related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is a main mechanism in prevention from oxidative stress, which may damage the nervous system. The present study employed this cell model to investigate whether Akt could induce axon growth in PC12 cells on the basis of NGF treatments. The results showed that Akt overexpression significantly increased cell proliferation and decreased cell apoptosis. Additionally, Akt overexpression activated Nrf2/ARE pathways. In conclusion, the experiments indicated that Akt overexpression contributed to axon regeneration induced by NGF in PC12 cells through activating the Nrf2/ARE pathway.

BackgroundHyperuricemia has a pathogenic role in the development of hypertension and other cardiovascular diseases (CVD). Uric acid has been reported to activate Nod-like receptor protein 3 (NLRP3)-inflammasome and alter vascular smooth muscle cells (VSMC). However, the potential mechanisms underlying this association are still not understood. The aim of this study was to investigate the role and potential mechanisms of uric acid in proliferation of VSMC.Material/MethodsCell Counting Kit-8 (CCK-8) proliferation assay and colony formation assay were performed to determine the proliferative ability of VSMC under uric acid stimulation. Immunofluorescence microscopy was carried out to determine the expression of Alpha-smooth muscle actin (α-SMA). In addition, real-time PCR and Western blot were used to detect the expression of NLRP3-inflammasome, and ELISA was performed to measure the levels of IL-18 and IL-1β.ResultsThe results showed that uric acid increases the proliferation of VSMC and induces α-SMA accumulation. We also found that uric acid increases the level of NLRP3 and induces NLRP3-inflammasome activation. The expressions of uric acid-induced inflammatory markers IL-1β and IL-18 were decreased by the inhibitor MCC950.ConclusionsOur findings revealed that uric acid induces inflammation through NLRP3-inflammasome-mediated VSMC proliferation. NLRP3 may be a new therapeutic target for hypertension.