Background: Effective prevention of jellyfish stings is crucial for human safety during marine activities. Traditional protective methods are often limited in terms of coverage area and duration of protection; Methods: This study designed and tested a novel jellyfish-repellent textile by coating waterproof polyester fabric with copper ion-loaded multicompartmental nanoparticles, which repel jellyfish by disrupting their cellular membranes and physiological functions. The nanoparticles were synthesized to enable spatial separation of components, enhance stability, and allow controlled copper ion release. They were applied to the fabric in one step via high-voltage electrostatic spray technology, followed by characterization using SEM and FT-IR. The copper sulfate release profile and nanoparticle adhesion were analyzed. Jellyfish-repellent efficacy was evaluated, along with biocompatibility tests including skin sensitization (Magnusson and Kligman method), skin irritation (Draize test), and cytotoxicity (MTT assay on L929 cells and human dermal fibroblasts). Results: SEM confirmed the formation of uniform multicompartmental nanoparticles with sizes ranging from 2.28 to 3.15 μm. FT-IR verified successful anchoring of Cu²⁺ ions to fabric fibers through coordination with hydroxyl groups. Drug release tests demonstrated water-triggered controlled release of copper ions lasting over 168 h, with nanoparticle retention rates exceeding 70% on all fabrics. The textile showed significant effectiveness in repelling jellyfish. Moreover, no apparent sensitization, irritation, or cytotoxicity was observed. Conclusions: A novel jellyfish-repellent textile was successfully developed using copper ion-loaded multicompartmental nanoparticles. This textile provides a promising solution for preventing jellyfish stings and contributes to the advancement of protective gear for marine activities.

Purpose: Bladder cancer (BC) is one of the top 10 common tumors in the world. It has been reported that microbiota can colonize tissues and play important roles in tumorigenesis and progression. However, the current understanding of microorganisms in the BC tissue microenvironment remains unclear.

Microbiota is present in the human tissue microenvironment and closely related to tumorigenesis and treatment. However, the landscape of tissue microbiome and its relationship with tumors remain less understood. In this study, we re-analyzed the omics data from the 7104 samples (94 projects for 15 cancers) in the NCBI database to obtain microbial profiles. After normalization and decontamination processing, we established classification models to distinguish between different tumors and tumor with adjacent normal tissues. The models had excellent performances, indicating that tissue microbiome had significant tumor specificity. Moreover, a series of key bacteria and bacteria-gene association pairs were screened out based on bioinformatic analysis, such as the tumor-promoting bacteria Fusobacterium, the tumor-suppressing bacteria Actinomyces, and the significant Rhodopseudomonas-COL1A1 association pair. In addition, we created a visual website, PTTM (http://198.46.152.196:7080/), for users to query and download the results. The identified key bacteria and association pairs provide candidate targets for further exploration of the molecular mechanisms of microbial action on tumorigenesis and the development of cancer therapy.

Background: Atopic dermatitis (AD) is a chronic skin condition marked by persistent itching and dryness. The role of cuproptosis, a novel form of programmed cell death, in AD is not yet understood.Methods: The GSE107361 dataset was obtained from the Gene Expression Omnibus (GEO) database. Cuproptosis-related genes (CRGs) in AD were identified and analyzed, and immune landscape analysis was performed using ssGSEA. AD was clustered based on CRGs using ConsensusClusterPlus. Weighted gene co-expression network analysis (WGCNA) and differential gene expression analysis were conducted. Hub genes between AD clusters were identified, and both protein-protein interaction (PPI) and drug-gene interaction networks were developed.Results: Three CRGs (DLD, MTF1, and GLS) were significantly upregulated in the AD group compared to healthy controls. Notably, four core CRGs (LIAS, LIPT1, PDHA1, CDKN2A) distinguished early-onset from adult-onset AD, indicating more active cuproptosis in early-onset AD. CRGs were linked to immune cell infiltration in AD, highlighting differences in immune microenvironments between early- and adult-onset AD. Early-onset AD showed high innate immunity, while adult-onset AD had a mix of innate and type 1 adaptive immunity. CRG expression identified two molecular subtypes with distinct immune infiltration: Cluster 2 (high cuproptosis) had predominant innate immunity, while Cluster 1 (low cuproptosis) had adaptive immunity. Additionally, 102 hub DEGs were identified through WGCNA co-expression network analysis, and 10 hub node genes were identified and potential drugs were explored for the management of AD.Conclusions: The study provides insights into the roles of cuproptosis-related processes in the pathogenesis and potential treatment of AD. Finding of key hub genes between the 2 distinct immune infiltration subtypes might inform potential therapeutic strategies for AD.

Basement membrane (BM) breaching is a critical hallmark of cutaneous squamous cell carcinoma (cSCC) invasion. This study aimed to identify novel BM-related genes (BMRGs) to effectively distinguish invasive cSCC from actinic keratosis (AK) and Bowen’s disease (BD), and to identify potential therapeutic targets. Single-cell RNA sequencing was used for BMRGs identification within keratinocytes and fibroblasts clusters. Protein–protein interaction network analysis and Lasso regression were performed for hub BMRGs screening, together with nomogram model construction and validation. In this study, 6–9 central hub BMRGs were identified for each stage during cSCC progression with a good AUC value (>0.8). In keratinocytes, BMRGs such as integrins (ITGB1, ITGA3, ITGA6), laminins (LAMA3, LAMC1), CD44, and FN1 were upregulated in cSCC compared to AK or BD (adjusted p < 0.05); in fibroblasts, BMRGs including ITGB1, ITGAV, LUM, BGN, SDC1, and FN1 were upregulated in cSCC (adjusted p < 0.05), suggesting their collective role in BM breaching and invasion, as well as a higher risk of BD. This study provides novel biological insights into the differentiation of progression pathways from AK or BD to cSCC, as well as potential targets for therapeutic intervention.