Purpose: We explored the reliability and validity of the Pain-related Beliefs and Attitudes about Sleep (PBAS) scale among patients with cancer. Further, we compared the usability of the PBAS scale with that of the Cancer-related Dysfunctional Beliefs and Attitudes about Sleep-14 (C-DBAS-14) among patients with cancer. Materials and Methods: The medical records of 252 patients with cancer who visited the sleep clinic from August 1, 2023 to June 30, 2024 were retrospectively analyzed. The responses of the enrolled patients to the PBAS, C-DBAS-14, Insomnia Severity Index (ISI), and Numeric Rating Scale of pain were collected. Results: The internal consistency reliability of the PBAS scale was excellent (Cronbach’s alpha of 0.96). Confirmatory factor analysis showed that the two-factor structure of the PBAS for patients with cancer is a good fit for the model (Comparative Fit Index, 0.99; Tucker-Lewis Index, 0.99; root mean square error of approximation, 0.14; standardized root mean square residual, 0.05). The convergent validity of the Korean version of the PBAS in patients with cancer was good, as indicated by its significant association with pain severity (r=0.63, p < 0.001), C-DBAS-14 (r=0.33, p < 0.001), and ISI (r=0.21, p < 0.01). The PBAS adequately reflected an increase in pain severity and was more effective and appropriate for capturing pain-related dysfunctional sleep beliefs than the C-DBAS-14. Conclusion The Korean version of the PBAS showed high reliability and validity in patients with cancer, and applicability across cancer types and cancer-related beliefs.

Cellular senescence causes cell cycle arrest and promotes permanent cessation of proliferation. Since the senescence of mesenchymal stem cells (MSCs) reduces proliferation and multipotency and increases immunogenicity, aged MSCs are not suitable for cell therapy. Therefore, it is important to inhibit cellular senescence in MSCs. It has recently been reported that metabolites can control aging diseases. Therefore, we aimed to identify novel metabolites that regulate the replicative senescence in MSCs. Using a fecal metabolites library, we identified nervonic acid (NA) as a candidate metabolite for replicative senescence regulation. In replicative senescent MSCs, NA reduced senescence-associated β-galactosidase positive cells, the expression of senescence-related genes, as well as increased stemness and adipogenesis. Moreover, in non-senescent MSCs, NA treatment delayed senescence caused by sequential subculture and promoted proliferation. We confirmed, for the first time, that NA delayed and inhibited cellular senescence.Considering optimal concentration, duration, and timing of drug treatment, NA is a novel potential metabolite that can be used in the development of technologies that regulate cellular senescence.