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Abstract Ulcerative colitis (UC) is characterised notably by an imbalance in intestinal mucosal homeostasis. Although mitochondrial dysfunction has been identified as a potential contributor to this imbalance, it remains an incomplete understanding. Consequently, further investigation into the role of mitochondria in UC is warranted. The study focusing on the GSE87466 dataset for differential gene expression analysis. Mitochondria-related genes were sourced from the MitoCart3.0 database. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to identify hub genes. The intersection of DEGs, hub genes, and mitochondria-related genes facilitated the identification of 14 mitochondria-related differentially expressed genes (MitoDEGs). Three machine learning algorithms were then applied to select signature MitoDEGs specific to UC: HMGCS2 and AMACR. They have decreased expression in UC patients and have a high diagnostic value for UC. In the inflammatory environment, knockout of both HMGCS2 and AMACR showed disruption of mitochondrial structure and function. Among them, the AMACR knockdown group had an increased number of damaged mitochondria and a significant reduction in the length, area and circumference of MAMs. Therefore, the study identified two new signature MitoDEGs in UC. HMGCS2 and AMACR provide insights into the interplay between mitochondrial dysfunction and UC intestinal mucosal homeostasis.

Abstract Ulcerative colitis (UC) is a chronic inflammatory condition of the intestinal tract. Various programmed cell death pathways in the intestinal mucosa are crucial to the pathogenesis of UC. Disulfidptosis, a recently identified form of programmed cell death, has not been extensively reported in the context of UC. This study evaluated the expression of disulfidptosis-related genes (DRGs) in UC through public databases and assessed disulfide accumulation in the intestinal mucosal tissues of UC patients and dextran sulfate sodium (DSS)-induced colitis mice via targeted metabolomics. We utilized various bioinformatics techniques to identify UC-specific disulfidptosis signature genes, analyze their potential functions, and investigate their association with immune cell infiltration in UC. The mRNA and protein expression levels of these signature genes were confirmed in the intestinal mucosa of DSS-induced colitis mice and UC patients. A total of 24 DRGs showed differential expression in UC. Our findings underscore the role of disulfide stress in UC. Four UC-related disulfidptosis signature genes—SLC7A11, LRPPRC, NDUFS1, and CD2AP—were identified. Their relationships with immune infiltration in UC were analyzed using CIBERSORT, and their expression levels were validated by quantitative real-time PCR and western blotting. This study provides further insights into their potential functions and explores their links to immune infiltration in UC. In summary, disulfidptosis, as a type of programmed cell death, may significantly influence the pathogenesis of UC by modulating the homeostasis of the intestinal mucosal barrier.

Abstract Solid polymer electrolytes (SPEs), which are favorable to form intimate interfacial contacts with electrodes, are promising electrolyte of choice for long-cycling lithium metal batteries (LMBs). However, typical SPEs with easily oxidized oxygen-bearing polar groups exhibit narrow electrochemical stability window (ESW), making it impractical to increase specific capacity and energy density of SPE based LMBs with charging cut-off voltage of 4.5 V or higher. Here, we apply a polyfluorinated crosslinker to enhance oxidation resistance of SPEs. The crosslinked network facilitates transmission of the inductive electron-withdrawing effect of polyfluorinated segments. As a result, polyfluorinated crosslinked SPE exhibits a wide ESW, and the Li|SPE|LiNi0.5Co0.2Mn0.3O2 cell with a cutoff voltage of 4.5 V delivers a high discharge specific capacity of ~164.19 mAh g−1 at 0.5 C and capacity retention of ~90% after 200 cycles. This work opens a direction in developing SPEs for long-cycling high-voltage LMBs by using polyfluorinated crosslinking strategy.

Abstract Nowadays, the increasing Dolichospermum (Anabaena) blooms pose a major threat to the aquatic environment and public health worldwide. The use of naturally derived chemicals from plants to control cyanobacteria blooms has recently received a tremendous amount of attention. This study investigates the possibility of transforming watermelon peel (WMP) into a biological resource to allelopathically inhibit Dolichospermum flos-aquae blooms. The results demonstrated that the growth of D. flos-aquae was efficiently restricted by the aqueous extract of watermelon peel (WMPAE) in a concentration-dependent manner. Cell viability decreased quickly, intracellular structural damage occurred, chlorophyll a in algal cells degraded, and photosynthesis was clearly inhibited. At the same time, the levels of reactive oxygen species in viable cells increased significantly, as did malondialdehyde levels, indicating that WMPAE elucidated strong oxidative stress and corresponding damage to D. flos-aquae. Capsular polysaccharide (CPS) levels increased in all treatment groups, which represents an adaptive response indicative of the development of resistance to WMPAE stress and oxidative damage. Despite this, WMPAE had clear inhibitory effects on D. flos-aquae. These findings provide fundamental information on an allelopathic system that could be a novel and attractive approach for suppressing D. flos-aquae blooms in small aquatic environments, especially aquaculture ponds.

While solid-state batteries offer higher energy densities than liquid-based batteries, such devices require effective ion conduction pathways. Here, authors prepare porous organic cages as solution-processable catholytes that are enable excellent performances from various cathode active materials.

Lan et al. report RNA structure ensembles across the entire SARSCoV-2 genome in infected human cells at single nucleotide resolution. They find alternative RNA conformations critical for promoting near-native frameshifting rates in ORF1ab.

Abstract Src homology 2 domain–containing inositol 5-phosphatase 1 (SHIP-1) regulates the intracellular levels of phosphotidylinositol-3, 4, 5-trisphosphate, a phosphoinositide 3–kinase (PI3K) product. Emerging evidence suggests that the PI3K pathway is involved in allergic inflammation in the lung. Germline or induced whole-body deletion of SHIP-1 in mice led to spontaneous type 2-dominated pulmonary inflammation, demonstrating that SHIP-1 is essential for lung homeostasis. However, the mechanisms by which SHIP-1 regulates lung inflammation and the responsible cell types are still unclear. Deletion of SHIP-1 selectively in B cells, T cells, dendritic cells (DC) or macrophages did not lead to spontaneous allergic inflammation in mice, suggesting that innate immune cells, particularly group 2 innate lymphoid cells (ILC2 cells) may play an important role in this process. We tested this idea using mice with deletion of SHIP-1 in the hematopoietic cell lineage and examined the changes in ILC2 cells. Conditional deletion of SHIP-1 in hematopoietic cells in Tek-Cre/SHIP-1 mice resulted in spontaneous pulmonary inflammation with features of type 2 immune responses and airway remodeling like those seen in mice with global deletion of SHIP-1. Furthermore, when compared to wild-type control mice, Tek-Cre/SHIP-1 mice displayed a significant increase in the number of IL-5/IL-13 producing ILC2 cells in the lung at baseline and after stimulation by allergen Papain. These findings provide some hints that PI3K signaling may play a role in ILC2 cell development at baseline and in response to allergen stimulation. SHIP-1 is required for maintaining lung homeostasis potentially by restraining ILC2 cells and type 2 inflammation.