Alzheimer's disease is characterized by the accumulation of beta-amyloid in plaques, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neurodegeneration and cognitive decline 1 . The NLRP3 inflammasome assembles inside of microglia upon activation, leading to increased cleavage and activity of caspase-1 and downstream IL-1β release 2 . While the NLRP3 inflammasome was shown to be essential for the development and progression of beta-amyloid pathology in mice 3 , the precise impact on tau pathology remains elusive. Here we show that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Tau activated the NLRP3 inflammasome and intracerebral injection of fibrillar beta-amyloid-containing brain *

Fuel cells and metal-air batteries will only become widely available in everyday life when the expensive platinum-based electrocatalysts used for the oxygen reduction reactions are replaced by other efficient, low-cost and stable catalysts. We report here the use of nitrogen-doped graphdiyne as a metal-free electrode with a comparable electrocatalytic activity to commercial Pt/C catalysts for the oxygen reduction reaction in alkaline fuel cells. Nitrogen-doped graphdiyne has a better stability and increased tolerance to the cross-over effect than conventional Pt/C catalysts.

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A bottom-up method is used to construct novel metal-free catalysts for deeper study of oxygen reduction reaction (ORR) catalysis. Through controlling the structural evolution of a 2D covalent triazine-based framework, the conductivity, nitrogen configurations, and multidoping structures of the as-prepared catalysts can be easily tuned, which makes a great platform for both studying the mechanisms of the ORR and optimizing the performances of the metal-free catalysts.

N, F co-doped graphdiyne was synthesized, which showed comparable electrocatalytic activity to Pt/C for ORR.

Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by the epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan.

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