RESUMO
Molybdenum oxide provides high theoretical capacity, but the moderate charge transfer kinetics and cycle life have limited the applications for capacitive energy storage. Herein, the electrochemical performance of molybdenum oxide is modified by tuning the active redox couple through an electrochemical activation process. The activated electrode K-MoOx with a 10 mg cm-2 loading shows excellent pseudocapacitive behavior within the large potential range of -1.2-0 V and delivers 313 F g-1 capacitance at 5 mA cm-2. It also presents an ultrastable cycle life, with a 98% capacitance retention after 10,000 cycles. The activation process involves the insertion of K+ into MoOx, which modifies the Mo electronic structure and introduces Mo4+ sites according to X-ray photoelectron spectroscopy. As a result, the charge storage redox couple shifts from Mo5+/Mo6+ to Mo4+/Mo5+, with the latter delivering higher electrochemical activity due to improved conductivity. Electrochemical impedance spectroscopy also suggests faster ion diffusions and thus higher power capability in K-MoOx, resulting in the enhanced performance. A 2.4 V asymmetric supercapacitor is assembled using K-MoOx as the anode with a MnOx cathode. The work demonstrates a feasible and facile strategy to promote the pseudocapacitive behavior of metal oxide materials.
RESUMO
A Na2SO4 + H2SO4 mixed electrolyte is demonstrated for a tungsten bronze pseudocapacitive electrode. The Na2SO4 supporting salt allows a large potential window while H+ effectively suppresses phase transformation. The electrode delivers a capacitance of 860 mF cm-2 with a -0.9 V-0 V window and 98% capacitance retention over 30 000 cycles.
RESUMO
AIM: To investigate the role of Δ133p53 isoform in nuclear factor-κB (NF-κB) inhibitor pyrrolidine dithiocarbamate (PDTC)-mediated growth inhibition of MKN45 gastric cancer cells. METHODS: The growth rate of MKN45 cells after treatment with different concentrations of only PDTC or PTDC in combination with cisplatin was detected by the CCK-8 assay. mRNA expression levels of Δ133p53, p53ß, and the NF-κB p65 subunit and p65 protein levels were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence, respectively. Growth of MKN45 cells was significantly inhibited by PDTC alone in a dose-dependent manner (P < 0.01). Moreover, the inhibitory effect of cisplatin was remarkably enhanced in a dose-dependent manner by co-treatment with PDTC (P < 0.01). RESULTS: RT-PCR analysis revealed that mRNA expression of p65 was curbed significantly in a dose-dependent manner by treatment with only PDTC (P < 0.01), and this suppressive effect was further enhanced when co-treated with cisplatin (P < 0.01). With respect to the other p53 isoforms, mRNA level of Δ133p53 was significantly reduced in a dose-dependent manner by treatment with only PDTC or PTDC in combination with cisplatin (P < 0.01), whereas p53ß mRNA expression was not altered by PDTC treatment (P > 0.05). A similar tendency of change in p65 protein expression, as observed for the corresponding mRNA, was detected by immunofluorescence analysis (P < 0.01). Pearson correlation analysis demonstrated that Δ133p53 and p65 mRNA expression levels were positively related, while no significant relationship was observed between those of p65 and p53ß (r = 0.076, P > 0.01). CONCLUSION: Δ133p53 isoform (not p53ß) is required in PDTC-induced inhibition of MKN45 gastric cancer cells, indicating that disturbance in the cross-talk between p53 and NF-κB pathways is a promising target in pharmaceutical research for the development of treatment strategies for gastric cancer.
