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Li||LiNi0.8Co0.1Mn0.1O2 batteries,which consist of lithium  metal anode (LMA) matched with NCM811 cathode, have an energy density more than twice that of lithium ion battery (LIB). However, the unstable electrode/electrolyte interface still hinders its practical application.Ether electrolytes show promise in improving the stability of LMA and NCM811 cathodes.However, a robust and stable electrode/electrolyte interface in Li||NCM811 batteries cannot be easily and efficiently achieved with most of the ether electrolytes reported in present studies. Herein, we present a straightforward and efficient tri-anion synergistic strategy to overcome this bottleneck. The addition of ClO4- and NO3- anions to LiFSI-based ether electrolytes forms a unique solvation structure with tri-anion (FSI-/ClO4-/NO3-) participation (LB511).This structure not only enhances the electrochemical window of the ether electrolytes but also achieves a stable Li||NCM811 batteries interface.The interaction between electrode and electrolyte is suppressed and an inorganic-rich (LiF/Li3N/LiCl) SEI/CEI layer is formed. Meanwhile, the coordination structure in the LB511 electrolyte increases the overpotential for Li deposition, resulting in a uniform and dense layer of deposition.Therefore, the Li||Cu cells using the LB511 electrolyte have an average CE of 99.6%.The Li||NCM811 batteries was cycled stably for 250 cycles with a capacity retention of 81% in the LB511 electrolyte (N/P = 2.5, 0.5 C)., (© 2024 Wiley‐VCH GmbH.)

Psoriasis is a common skin disease with a high recurrence rate. Aberrant keratinocyte proliferation is a significant pathogenic characteristic of psoriatic lesions, and studies have revealed that the development of psoriasis is significantly influenced by pro-inflammatory cytokines, such as IL-17A and TNF-α. Biologics targeting these cytokines have been widely used in psoriasis treatment and achieve remarkable effects, however, the underlying mechanism of how IL-17A and TNF-α specifically regulate keratinocyte proliferation has not been fully elucidated. Dectin-1 is an essential membrane protein that is directly related to the immune microenvironment and the proliferation of multiple cell types. To elucidate how IL-17A and TNF-α may promote keratinocyte proliferation in psoriatic lesions and whether Dectin-1 is involved. The expression of Dectin-1 in keratinocytes from psoriatic lesions was detected by real-time PCR, western blot and immunofluorescence. Correlation analysis and cytological experiments were then performed to determine the relationship between Dectin-1 and IL-17A/TNF-α in psoriatic lesions. Finally, we investigated the signalling pathway through which Dectin-1 may promote keratinocyte proliferation. Dectin-1 was significantly increased in keratinocytes from psoriatic lesions. Moreover, IL-17A and TNF-α effectively induced the expression of Dectin-1 in HaCaT cells, which was shown to activate the Syk/NF-κB signalling pathway and promote the proliferation of keratinocytes. IL-17A and TNF-α may promote the proliferation of keratinocytes in psoriatic lesions through induction of Dectin-1, indicating that Dectin-1 could be a potential therapeutic target for the treatment of psoriasis.