To explore the correlation between Fried Frailty Phenotype (FFP) and the muscle thickness and quality of local muscle, and to provide a reasonable basis for the application of ultrasound measurement in the frailty assessment. A total of 150 people (age ≥ 65 years, 58 women, 92 men) were included from the First Hospital Affiliated to Nanjing Medical University. They were divided into Normal group (40 cases), Prefrailty group (69 cases) and Frailty group (41 cases). The thickness and the quality of local muscle were detected by ultrasound. Participants in the prefrailty group had a higher grayscale value of the vastus lateralis muscle, indicating the deterioration of muscle quality. At the frailty stage, the muscle thickness and quality of the vastus lateralis muscle and the anterior tibialis muscle decreased significantly compared with the normal and the prefrailty group. Pearson's correlation analysis also showed FFP was negatively correlated with muscle thickness and quality of the lower limbs. In multiple regression model, FFP was positively associated with gray value (Vastus lateralis muscle:β =0.457, p < 0.001; Anterior tibialis muscle: β = 0.220, p = 0.037) and inversely associated with muscle thickness (Vastus lateralis muscle:β = −0.973, p = 0.031; Anterior tibialis muscle: β = −4.551, p = 0.004) in the frailty stage. Together, FFP was closely related to muscle thickness and quality, especially vastus lateralis muscle. Moreover, Muscle quality has deteriorated in the prefrailty stage, which is earlier than muscle thickness.

Docetaxel resistance seriously affects its clinical application in prostate cancer (PCa). Ferroptosis is a type of iron-dependent cell death driven by lipid peroxidation. It has been recently found that ferroptosis influences various biological processes. However, the potential role of ferroptosis in docetaxel chemotherapy for PCa is still elusive. In this study, we aimed to explore whether altering the level of ferroptosis can affect docetaxel sensitivity in PCa. The results indicated that docetaxel promoted ferroptotic cell death in several PCa cells, and ferroptosis inducers, erastin, and RSL3 markedly increased the cytotoxic effect of docetaxel. Furthermore, our results showed that ferroptosis resistance was closely associated with docetaxel insensitivity in PCa-resistant cells. Erastin or RSL3 rendered resistant PCa cells susceptible to docetaxel, with elevated levels of lipid ROS and decreased protein expression of GPX4 and SLC7A11. Moreover, treatment with erastin and RSL3 led to significant suppression of resistant tumors, and the combination of RSL3 with docetaxel significantly halted tumor growth in vivo when compared with either drug. Taken together, our findings indicate that ferroptosis is involved in docetaxel resistance, and its inducers are promising therapeutic strategies for advanced PCa.