Synergistic effect of protein foams and polysaccharide on the invisible hemostasis of acellular dermal matrix sponges.

Efficient management of hemorrhage is vital for preventing hemorrhagic shock and safeguarding wounds against infection. Inspired by the traditional Chinese steamed bread-making process, which involves kneading, foaming, and steaming, we devised a hemostatic sponge by amalgamating an acellular dermal matrix gel, hydroxyethyl starch, and rice hydrolyzed protein. The integration of hydroxyethyl starch bolstered the sponge's mechanical and hemostatic attributes, while the inclusion of rice hydrolyzed protein, acting as a natural foaming agent, enhanced its porosity This augmentation facilitated rapid blood absorption, accelerated clot formation, and stimulated the clotting cascade. Experimental findings underscore the exceptional biocompatibility and physicochemical characteristics of the hemostatic sponge, positioning it on par with commercially available collagen hemostatic sponges for hemorrhage control. Mechanistically, the sponge fosters aggregation and activation of red blood cells and platelets, expediting coagulation kinetics both in vivo and in vitro. Notably, this hemostatic sponge activates the clotting cascade sans crosslinking agents, offering a premium yet cost-effective biomaterial with promising clinical applicability.

AMPK activation eliminates senescent cells in diabetic wound by inducing NCOA4 mediated ferritinophagy.

BACKGROUND: Diabetic wounds are one of the long-term complications of diabetes, with a disordered microenvironment, diabetic wounds can easily develop into chronic non-healing wounds, which can impose a significant burden on healthcare. In diabetic condition, senescent cells accumulate in the wound area and suppress the wound healing process. AMPK, as a molecule related to metabolism, has a close relationship with aging and diabetes. The purpose of this study was to investigate the effects of AMPK activation on wound healing and explore the underlying mechanisms. METHODS: AMPK activator A769662 was topically applied in wound models of diabetic mice. Alterations in the wound site were observed and analyzed by immunohistochemistry. The markers related to autophagy and ferritinophagy were analyzed by western blotting and immunofluorescence staining. The role of AMPK activation and ferritinophagy were also analyzed by western blotting. RESULTS: Our results show that AMPK activation improved diabetic wound healing and reduced the accumulation of senescent cells. Intriguingly, we found that AMPK activation-induced ferroptosis is autophagy-dependent. We detected that the level of ferritin had deceased and NCOA4 was markedly increased after AMPK activation treatment. We further investigated that NCOA4-mediated ferritinophagy was involved in ferroptosis triggered by AMPK activation. Most importantly, AMPK activation can reverse the ferroptosis-insensitive of senescent fibroblast cells in diabetic mice wound area and promote wound healing. CONCLUSIONS: These results suggest that activating AMPK can promote diabetic wound healing by reversing the ferroptosis-insensitive of senescent fibroblast cells. AMPK may serve as a regulatory factor in senescent cells in the diabetic wound area, therefore AMPK activation can become a promising therapeutic method for diabetic non-healing wounds.

Efficacy of Diffusion-Weighted Imaging in Neoadjuvant Chemotherapy for Osteosarcoma: A Systematic Review and Meta-Analysis.

RATIONALE AND OBJECTIVES: Diffusion-weighted imaging (DWI) is a noninvasive imaging technique that reflects the diffusion movement of water molecules through apparent diffusion coefficient (ADC) values. The role of DWI in predicting the histological response to neoadjuvant chemotherapy in osteosarcoma is being increasingly researched, and a systematic review and meta-analysis of this topic is urgently required to help determine the potential diagnostic value of DWI. MATERIALS AND METHODS: The present meta-analysis included 13 studies (303 patients). We divided the target population into good responders and poor responders based on tumor necrosis on histological biopsy (≥90%, good responders). The mean ADC values and ADC ratio were extracted and/or calculated for the two groups. RESULTS: The mean difference in ADC values before and after neoadjuvant chemotherapy was significantly higher in good responders than in poor responders (mean difference, 0.33; 95% confidence interval [CI], 0.18-0.49; p< 0.0001), and significant heterogeneity was present among the 10 studies that reported these values (I2 = 66%, p< 0.05). The ADC ratio was also significantly higher in good responders than in poor responders (mean difference, 28.34; 95% CI, 1.83-54.85; p = 0.04), and significant heterogeneity in ADC ratio was present among 7 studies (I2 = 97%, p< 0.05). CONCLUSION: The mean differences in ADC values and ADC ratios before and after neoadjuvant chemotherapy for osteosarcoma were significantly higher in good responders than in poor responders.