Background: To explore the effects of risk factors-based nursing management on the occurrence of pressure sores in hospitalized patients. Methods: From Jan 2018 to Jun 2018, 289 hospitalized patients were divided into pressure sores group [100] and control group [189] for retrospective analysis. Overall, 260 hospitalized patients from Jun 2018 to Dec 2018 were followed up for nursing intervention. Overall 130 patients received risk factors-based nursing case management were in the intervention group, whereas 130 patients who received routine nursing care were in the control group. The chi-square test and t-test were used to compare the count data and the measurement data between groups, respectively. Results: Age, body weight and proportions of patients with impaired nutritional intake, diabetes or stroke in pressure sores group were higher than those in normal group (P<0.05). Hospital stay and operative time in pressure sores group was longer than those in normal group (P<0.05). The frequency of assistant activity in pressure sores group was significantly lower than that in control group (P<0.05).In addition, the score of uroclepsia in pressure sores group was lower than that in normal group (P<0.05). Patients in the intervention group showed lower risk for pressure sores and more satisfied than patients in control group (P<0.001). Conclusion: Advanced age, high body weight, diabetes and stroke, long hospital stay, long operative time, poor nutritional status and severe uroclepsia were independent risk factors of pressure sores. Risk factorsbased nursing case management can effectively reduce the occurrence and risk of pressure sores for hospitalized patients.

Excessive inflammation and metabolic dysregulation fuel alveolar cell death in sepsis-induced lung injury, yet effective molecular interventions are lacking. We identify citrate lyase beta-like (CLYBL) as a previously unrecognized metabolic driver of macrophage-mediated tissue damage. In a murine cecal ligation and puncture model, CLYBL was strongly upregulated in lung tissue and peritoneal macrophages. To therapeutically target this pathway, we engineered platelet-derived extracellular vesicle–coated poly(lactic-co-glycolic acid) nanoparticles (PEVs@PLGA) encapsulating CLYBL-specific small interfering RNA. This platelet-mimetic system enabled efficient, biocompatible delivery of siRNA and robust CLYBL knockdown both in vitro and in vivo. CLYBL silencing triggered accumulation of the anti-inflammatory metabolite itaconate, limited M1 macrophage polarization, and preserved alveolar epithelial integrity, thereby reducing cell death and improving pulmonary repair. Transcriptomic analysis revealed broad immunometabolic remodeling consistent with enhanced resolution of inflammation. Biosafety evaluation confirmed negligible systemic toxicity. These findings uncover CLYBL as a critical metabolic checkpoint linking macrophage activation to alveolar cell death and highlight platelet-mimetic siRNA nanoparticles as a potent therapeutic strategy. Our work provides a mechanistic and translational framework for targeting macrophage immunometabolism to prevent fatal organ damage during sepsis.

Sepsis-induced acute lung injury (ALI) is a critical clinical condition characterized by severe inflammation and alveolar epithelial barrier disruption, with limited effective treatments. Our study investigates the role of Sbno2-expressing tissue-resident alveolar macrophages (TR-AMs) in promoting alveolar epithelial cell (AEC) regeneration and barrier function in sepsis-induced ALI. Utilizing single-cell RNA sequencing (scRNA-seq), we identified significant upregulation of Sbno2 in TR-AMs, which correlated with enhanced AEC proliferation and reduced apoptosis. Functional assays demonstrated that Sbno2-expressing TR-AMs substantially supported alveolar structure regeneration in both in vitro and in vivo models. Knockout of Sbno2 in TR-AMs impaired AEC proliferation and compromised lung barrier integrity. Therapeutic administration of recombinant Sbno2 (rSbno2) in a sepsis-induced ALI mouse model alleviated lung injury, promoted AEC proliferation, and restored barrier function, highlighting Sbno2 as a potential therapeutic target for ALI. These findings provide novel insights into the molecular mechanisms of lung repair in sepsis-induced ALI and suggest that enhancing Sbno2 expression in TR-AMs could be a promising strategy for improving outcomes in patients with ALI.

This study identifies the V-set domain-containing T-cell activation inhibitor 1 (VTCN1)–galectin-3 axis as a key immunosuppressive pathway in colorectal cancer (CRC). We show that inhibiting VTCN1 downregulates galectin-3 in T cells, reversing their dysfunction and reactivating antitumor immunity. Therapeutically, the VTCN1 inhibitor SGN-B7H4 restricted tumor progression by enhancing T-cell activity and impairing cancer cell proliferation, migration, and invasion. These findings reveal a novel immune checkpoint mechanism and establish VTCN1 as a promising target to overcome immunotherapy resistance in CRC.