Objective To investigate the role of SLC7A11-mediated disulfidptosis in regulating the functional heterogeneity of cancer-associated fibroblasts (CAFs) and remodeling the immune microenvironment in ovarian cancer (OC). Methods Utilizing an integrative multi-omics framework, we synchronized transcriptomic data from TCGA and GEO with high-resolution single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics. We employed CellChat interactome algorithms to map disulfidptosis-related gene expression profiles across various cellular hierarchies. The mechanistic link between SLC7A11 and SPP1 was further examined via qPCR assays under glucose-deprived, disulfidptosis-inducing conditions. Results SLC7A11 was identified as a crucial regulator of disulfidptosis, exhibiting significant overexpression in OC tissues. Elevated SLC7A11 levels were positively correlated with advanced FIGO stages, increased tumor burden, and resistance to immune checkpoint blockade. scRNA-seq profiling identified a distinct CAF lineage (CAF1/CAF5) characterized by a robust disulfidptosis signature. This subpopulation was associated with epithelial-mesenchymal transition and an immunosuppressive niche via the SPP1-CD44 signaling axis. In situ spatial mapping suggested the localized amplification of SPP1-mediated signaling at the CAF-tumor cell interface, forming high-intensity interactomes with ITGAV, ITGB1, and CD44. Metabolic stress induced by glucose starvation significantly altered the transcriptional profiles of SLC7A11 and SPP1. Notably, the glucose starvation-induced upregulation of NRF2 mRNA in fibroblasts was effectively mitigated by NRF2 knockdown or treatment with the disulfidptosis inhibitor 2-mercaptoethanol. Conclusion SLC7A11-mediated disulfidptosis may activates a subset of CAFs, which may contribute to remodeling the tumor microenvironment and suppressing anti-tumor immunity through the secretion of SPP1.

Eight new diaryltriazine derivatives containing 4-allylamino and 4-azido substitutes guided by molecular docking have been designed and synthesized based on our previous work.The evaluation of HIV inhibitory activity demonstrated that all compounds were potent against HIV-1 replication.The most active compound 7c exhibited activity against HIV-1 (IC50=0.034 μmol·L-1,SI=6475)and the double mutant strain (IC50=9.39 μmol·L-1)in the micromolar range, which was more potent than nevirapine.

Purpose　The aim is to develop a synthesis method of the silver carboxymethyl chitosan and to study its bacteriostasis to Staphlococcus aureus(S.aureus),Pseudomonas aeruginusa(P.aeruginusa),Escherichia Coli(E.coli),Klebsiella pneumoniae(K.pneumoniae) and Proteus vulgaris(P.vulgaris).Methods　Chitosan was modified by way of chemistry.The structure analysis of its derivate was analysed by infra-red absorption spectroscopy,using methods of dilution and concavering to study the bacteriostasis to some ordinary bacteria which cause infection in burn.Results　The infra-red spectragram of the derivate showed the chitosan had been modified by chloroacetic acid.When the concentrationl of silver carboxymethyl chitosan was 1.028 mg/ml and the concentration of the five bacteria were 104CFU/ml，the rate of bacteriostasis was 88%、80.2%、75.3% to S.aureus、P.aeruginusa and E.coli respectively.The MIC of silver carboxymethyl chitosan was similar to that of AgNO3 when they act on S.aureus and P.aeruginusa,but the former was lower than later when acting on E.coli.Conclusion　Silver carboxymethyl chitosan could inhibit some bacteria which caused infection in burn.It was a novel pharmaceutical in preventing and curing burn infection.