Lithium–sulfur (Li–S) batteries are regarded as one of the promising energy storage systems. However, rapid capacity attenuation caused by shuttle effect of soluble polysulfides is major challenge in practical application. The separator modification is regarded as one countermeasure besides the construction of sulfur host materials. Covalent organic frameworks (COFs) are one type of outstanding candidates for suppressing shuttle effect of polysulfides. Herein, recent advances of COFs in the application as commercial separator modifiers are summarized. COFs serve as ionic sieves, the importance of porous size and surface environments in inhibiting soluble polysulfides shuttling and promoting lithium ions conduction is highlighted. The superiority of charge‐neutral COFs, ionic COFs, and the composites of COFs with conductive materials for improving reversible capacity and cycling stability is demonstrated. Some new strategies for the design of COF‐based separator modifiers are proposed to achieving high energy density. The review provides new perspectives for future development of high‐performance Li–S batteries.

Here we report the discovery and identification of antibacterial substances from the secondary metabolites of a new strain Bacillus velezensis BA-26. The whole genome of B. velezensis BA-26 was sequenced. Its genome data were annotated, and four potentially unknown gene clusters and nine known secondary metabolite synthetic gene clusters were analyzed and excavated by antiSMASH software. Based on the predicted secondary metabolites from the genome of strain BA-26, the material identification of isolated and purified extracellular secondary metabolites was conducted in combination with mass spectrometry data. A total of 24 antifungal compounds were identified, namely, iturin and various fengycins. The minimum inhibitory concentration (MIC) of iturin to Botrytis cinerea was 62.50 µg•mL −1 . The MICs of C 14 fengycin A, C 16 fengycin A and C 18 fengycin A were 62.50, 31.25 and 0.49 µg•mL −1 , respectively, indicating that the increase in the number of carbon atoms in side chain fatty acids of fengycin improves its biological activity. Two kinds of anti-disease fungal compounds from B. velezensis BA-26, namely, iturin and fengycin, were purified and identified; they were found to have antibacterial activities against common pathogenic fungi. Therefore, B. velezensis BA-26 may be potentially used as a biological control agent. This study enriches the genome information on B. velezensis, elucidates the active components of B. velezensis BA-26 antibacterial substances, and provides a useful reference for using strain BA-26 as a biological control agent.

Terrestrosin D (TED) is the active ingredient of Tribulus terrestris L., which is used in traditional Chinese medicine (TCM) formulations and has a wide range of pharmacological activities. A previous study showed that TED alleviated bleomycin (BLM)‐induced pulmonary fibrosis (PF) in mice. However, the mechanisms underlying the therapeutic effect of TED are still unclear and need further investigation. In this study, we evaluated the effect of TED in a mice of BLM‐induced PF in terms of histopathological and biochemical indices. UHPLC–MS‐based plasma metabolomics combined with network pharmacology was used to explore the pathological basis of PF and the mechanism of action of TED. Histological and biochemical analyses showed that TED mitigated inflammatory injury in the lungs, especially at the dosage of 20 mg/kg. Furthermore, BLM changed the plasma metabolite profile in the mice, which was reversed by TED via regulation of amino acid and lipid metabolism. Subsequently, a biomarkers‐targets‐disease network was constructed, and tumor necrosis factor (TNF)‐α and transforming growth factor (TGF)‐β1 were identified as the putative therapeutic targets of TED. Both factors were quantitatively analyzed using enzyme‐linked immunosorbent assay (ELISA). Taken together, the combination of UHPLC–MS‐based metabolomics and network pharmacology can unveil the mechanisms of diseases and drug action.

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