Conjugated microporous polymers (CMPs) rank among the most promising materials for sustainable lithium-ion batteries (LIBs) in terms of their tunable chemical structures and designable electrochemical performance. Herein, a CMP of poly(anthraquinone-co-hexaazatriphenylene) (PAQ-HATN) was synthesized by combining anthraquinone (AQ) with a highly active hexaazatriphenylene (HATN) group, which is endowed with abundant redox-active groups, high specific surface area, and insolubility in an electrolyte. Further, to address the existing problems of PAQ-HATN, including poor rate performance, low conductivity, and structural instability, the strategy through the integration of an organic polymer (PAQ-HATN) with inorganic material (TiS2) was used. The prepared composite as a cathode material (PAQ-HATN@TiS2) achieves improved conductivity and effective utilization of the redox activity sites. As expected, PAQ-HATN@TiS2 exhibits high initial capacity (347.6 mA h g–1 at 25 mA g–1), good rate performance (114.8 mA h g–1 at 1000 mA g–1), and long cycle stability (157.4 mA h g–1 at 800 mA g–1 and 1000th cycle), indicating the PAQ-HATN@TiS2 compound is a potential cathode for energy storage.
This research focused on how upregulation of S100A9 contributed to the pathogenesis of the dry eye disease (DED) and whether S100A9 served as a promising therapeutic target in DED. Public single-cell RNA sequencing (scRNA-seq) data of a lacrimal gland excision (LGE) murine DED model was analyzed. LGE model was established and expression of protein was measured through immunofluorescence and western blot. DED-related signs were evaluated through tear secretion and fluorescent staining. TUNEL was performed to detect the level of cell death. Briefly, S100A9 was recognized as a highly variable gene in the DED group. LGE model was successfully established, and S100A9 showed a time-dependent increase in the corneal epithelia. Autophagic blockage was predicted by the scRNA-seq data in DED, and further verified by decrease of LC3B-II/LC3B-I and increase of SQSTM1 and p-mTOR/mTOR, while S100A9 inhibitor paquinimod (PAQ) reversed the changes. PAQ also downregulated TLR4, and inhibition of TLR4 also alleviated autophagic blockage in DED. Finally, signs of DED, chronic corneal inflammation and cell death got a remission after either inhibition of S100A9 or TLR4. In general, we deduced a S100A9-TLR4-Autophagic blockage pathway in the pathogenesis of DED.
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