RESUMO
Objective: This study investigated the impact of the flap vascular pressurization technique on repairing large-area soft tissue defects in the limbs. Methods: This study employed a randomized controlled trial design to enroll patients with large-area skin defects in the limbs, accompanied by exposed deep tissues such as nerves, blood vessels, bones, and tendons, for various reasons between July 2020 to July 2022. The patients were randomly assigned into two groups using a random number table method. The control group (n = 30) underwent traditional anterior lateral thigh flap repair, while the experimental group (n = 30) underwent flap repair using the vascular pressurization technique. Clinical indicators, flap survival, scar formation, and satisfaction were compared between the two groups. Results: There were no significant differences in operation time, intraoperative blood loss, and length of hospital stay between the two groups (P > .05). The flap survival rate in the experimental group (90.00%, 27/30) was significantly higher than that in the control group (66.67%, 20/30) (P < .05). The Manchester Scar Scale (MSS) scores in the experimental group were significantly higher than those in the control group (P < .05). The satisfaction rate in the experimental group (93.33%, 28/30) was significantly higher than that in the control group (73.33%, 22/30) (P < .05). Conclusion: The use of the flap vascular pressurization technique for the repair of soft tissue defects in the limbs can significantly increase flap survival rate, improve scar formation, and enhance patient satisfaction, thereby demonstrating good clinical value. The flap vascular pressurization technique can be promoted as a reliable method for repairing large-area skin defects in the limbs, thereby contributing to the advancement of specialized fields.
Assuntos
Procedimentos de Cirurgia Plástica , Lesões dos Tecidos Moles , Humanos , Cicatriz/cirurgia , Lesões dos Tecidos Moles/cirurgia , Resultado do Tratamento , Transplante de PeleRESUMO
BACKGROUND: Oridonin is a powerful anticancer compound found in Rabdosia rubescens. However, its potential impact on bladder cancer remains uninvestigated. In this work, we aimed to detect the anticancer effect of oridonin on bladder cancer and explore the molecular mechanisms involved. METHODS: The anticancer activity of oridonin was assessed in vitro with a CCK8 assay, an annexin V-FITC apoptosis analysis, and colony formation and Transwell migration assays which were performed with the human bladder cancer cell line T24. Levels of apoptosis-related proteins, melastatin transient receptor potential channel 7 (TRPM7), and signaling molecules were examined in oridonin-treated T24 cells by western blotting or RT-PCR. Oridonin anticancer efficacy was further validated in vivo with a T24 xenograft mouse model. RESULTS: Oridonin repressed the proliferative, colony-forming, and migratory capacities of T24 cells, triggered extensive apoptosis in vitro, and retarded tumor growth in vivo. Moreover, oridonin treatment significantly increased expression levels of p53 and cleaved caspase-3 and reduced expression of TRPM7, p-AKT, and p-ERK. CONCLUSION: Oridonin exhibited outstanding antiproliferative and antimigratory effects on bladder cancer, and these effects were at least partially associated with targeting of TRPM7 through inactivation of the ERK and AKT signaling pathways. These findings provide insight for the clinical application of oridonin in bladder cancer prevention.