All-solid-state lithium ion batteries (LIBs) are ideal for energy storage given their safety and long-term stability. However, there is a limited availability of viable electrode active materials. Herein, we report a truxenone-based covalent organic framework (COF-TRO) as cathode materials for allsolid-state LIBs. The high-density carbonyl groups combined with the ordered crystalline COF structure greatly facilitate lithium ion storage via reversible redox reactions. As a result, a high specific capacity of 268 mAh g À1 , almost 97.5 % of the calculated theoretical capacity was achieved. To the best of our knowledge, this is the highest capacity among all COF-based cathode materials for all-solid-state LIBs reported so far. Moreover, the excellent cycling stability (99.9 % capacity retention after 100 cycles at 0.1 C rate) shown by COF-TRO suggests such truxenone-based COFs have great potential in energy storage applications.

[100] is believed to be a tough diffusion direction for Li(+) in LiFePO4, leading to the belief that the rate performance of [100]-oriented LiFePO4 is poor. Here we report the fabrication of 12 nm-thick [100]-oriented LiFePO4 nanoflakes by a simple one-pot solvothermal method. The nanoflakes exhibit unexpectedly excellent electrochemical performance, in stark contrast to what was previously believed. Such an exceptional result is attributed to a decreased thermodynamic transformation barrier height (Δμb) associated with increased active population.

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Oxidative stress is a key mechanism underlying ozone-induced lung injury. Mitochondria can release mitochondrial reactive oxidative species (mtROS), which may lead to the activation of NLRP3 inflammasome. The goal of this study was to examine the roles of mtROS and NLRP3 inflammasome in acute ozone-induced airway inflammation and bronchial hyperresponsiveness (BHR). C57/BL6 mice (n=8/group)were intraperitoneally treated with vehicle (phosphate buffered saline, PBS) or Mito-TEMPO (mtROS inhibitor, 20mg/Kg), or orally treated with VX-765 (caspse-1 inhibitor, 100mg/Kg) one hour before the ozone exposure (2.5ppm, 3 hour). Compared to PBS-treated ozone-exposed mice, MitoTEMPO reduced the level of total malondialdehyde in bronchoalveolar lavage (BAL) fluid and increased the expression of mitochondrial complexes II and IV in the lung 24-hour after single ozone exposure. VX-765 inhibited ozone-induced BHR, BAL total cells including neutrophils and eosinophils and BAL inflammatory cytokines including IL-1α、IL-1β、KC and IL-6. Both MitoTEMPO and VX-765 reduced ozone-induced mtROS and inhibited capase-1 activity in lung tissue whilst VX-765 further inhibited DRP1 and MFF expression, increased MFN2 expression and down-regulated caspase-1 expression in lung tissue. These results indicate that acute ozone exposure induces mitochondrial dysfunction and NLRP3 inflammasome activation, while the latter has a critical role in the pathogenesis of ozone induced airway inflammation and BHR.