Massive bleeding and wound infection are the major problems often observed during severe trauma, and achieving rapid hemostasis in cases of high‐dose bleeding in arteries and viscera remains an acute clinical demand. Herein, a mussel‐ and barnacle cement proteins‐inspired dual‐bionic hydrogel is first proposed. Benefiting from abundant phenolic hydroxyl groups, a tough dissipative matrix, removal of interfacial water, as well as dynamic redox balance of phenol‐quinone, the multinetwork hydrogel achieves repeatable robust wet‐tissue adhesiveness (151.40 ± 1.50 kPa), a fast multimodal self‐healing ability, and excellent antibacterial property against both Gram‐positive/negative bacteria. For rabbit/pig models of cardiac penetration holes and femoral artery injuries, the dual‐bionic bioadhesive shows better hemostatic efficiency than commercial gauze due to the synergistic effect of strong wound sealing capability, excellent red blood cell capturing property, and activation of hemostatic barrier membrane. More interestingly, the hydrogel combined with commercial hemostatic sponge presents accelerated wound healing as well as great potential for treating deep‐wound hemorrhage in a battlefield environment. Overall, owing to these unique advantages, the novel tissue‐adhesive hemostat opens up a new avenue to rapid sealing hemostasis and wound healing applications.
This study aimed to probe carcinogenic genes and pathways associated with Wilms' tumor (WT) onset and malignancy progression. After screening, three datasets acquired from the Gene Expression Omnibus database were analyzed. Differentially expressed genes (DEGs) were identified and GO functional enrichment, KEGG pathway enrichment and protein-protein interaction (PPI) were analyzed. The DEGs with top fold change values or top protein interaction scores were used to analyze overall survival based on the TARGET WT dataset. Together, 866 up-regulated genes in GDS1791, 585 up-regulated genes in GDS2010, and 277 down-regulated genes in GDS4802 were found, from which 46 key DEGs were selected for further analysis. In the PPI network, hub positions included COL5A1, COL4A1, ARPP21, SPARCL1, CD86, LY96 and PPP1R12B. The top DEGs (ARPP21, SYNPO, PRRC2B, PPP1R12B, EFCAB2 and LY96) were selected for survival analysis, and they consistently showed a significantly positive correlation with poor survival. Together, five key carcinogenic genes (SYNPO, PRRC2B, PPP1R12B, EFCAB2 and LY96) were highly associated with WT onset and patient survival. These risk genes, interaction networks and enrichments should improve our understanding of the complex molecular mechanisms in WT development and help clinical applications.
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