The main challenges to the commercial viability of polymer electrolyte membrane fuel cells are (i) the high cost associated with using large amounts of Pt in fuel cell cathodes to compensate for the sluggish kinetics of the oxygen reduction reaction, (ii) catalyst degradation, and (iii) carbon-support corrosion. To address these obstacles, our group has focused on robust, carbon-free transition metal nitride materials with low Pt content that exhibit tunable physical and catalytic properties. Here, we report on the high performance of a novel catalyst with low Pt content, prepared by placing several layers of Pt atoms on nanoparticles of titanium nickel binary nitride. For the ORR, the catalyst exhibited a more than 400% and 200% increase in mass activity and specific activity, respectively, compared with the commercial Pt/C catalyst. It also showed excellent stability/durability, experiencing only a slight performance loss after 10,000 potential cycles, while TEM results showed its structure had remained intact. The catalyst's outstanding performance may have resulted from the ultrahigh dispersion of Pt (several atomic layers coated on the nitride nanoparticles), and the excellent stability/durability may have been due to the good stability of nitride and synergetic effects between ultrathin Pt layer and the robust TiNiN support.

N,P co-doped porous carbon as a highly efficient electrocatalyst for N2 fixation in aqueous solution under ambient conditions.

Background: Identifying effective drugs to suppress vascular inflammation is a promising strategy to delay the progression of abdominal aortic aneurysm (AAA). Itaconate has a vital role in regulating inflammatory activation in various inflammatory diseases. However, the role of itaconate in the progression of AAA is unknown. In this study, we explored the inhibitory effect of itaconate on AAA formation and its underlying mechanisms. Methods: Quantitative PCR, western blotting and immunohistochemistry were used to determine Irg1 and downstream Nrf2 expression in human and mouse AAA samples. Liquid chromatograph-mass spectrometry (LC-MS) analysis was performed to measure the abundance of itaconate. OI treatment and Irg1 knockdown were performed to study the role of OI in AAA formation. Nrf2 intervention in vivo was performed to detect the critical role of Nrf2 in the beneficial effect of OI on AAA. Findings: We found that itaconate suppressed the formation of angiotensin II (Ang II)-induced AAA in apolipoprotein E-deficient (Apoe À/À ) mice, while Irg1 deficiency exerted the opposite effect. Mechanistically, itaconate inhibited vascular inflammation by enabling Nrf2 to function as a transcriptional repressor of downstream inflammatory genes via alkylation of Keap1. Moreover, Nrf2 deficiency significantly aggravated inflammatory factor expression and promoted AAA formation. In addition, Keap1 overexpression significantly promoted Ang II-induced AAA formation, which was inhibited by itaconate. Interpretation: Itaconate inhibited AAA formation by suppressing vascular inflammation, and therapeutic approaches to increase itaconate are potentially beneficial for preventing AAA formation.

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