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BACKGROUND: In 2021, China had a population of 264·01 million individuals over the age of 60, indicating a high prevalence of chronic diseases. Among older adults, physical inactivity (PI) is a significant risk factor for chronic diseases. However, few studies have been conducted on the correlation of physical activity (PA) with the economic status, geography and chronic disease risks in Chinese elderly. The objectives of this study were to better understand the distribution of PA among older adults in China and its relationship with economic status, geography, and chronic disease risks. METHODS: This study utilized data from the China Longitudinal Aging Social Survey (CLASS) in 2020, post-COVID-19. The study employed a stratified, multistage, probabilistic sampling approach and included 11,396 adults over the age of 59 from 28 provinces in China. Data on demographics, the duration and intensity of PA, history of diseases and personalized factors influencing PA were collected via structured interviews by researchers. In this study, we conducted a comprehensive analysis, employing a range of statistical methods including descriptive analysis, Wilcoxon rank-sum tests, Bayesian networks, and chi-square tests. RESULTS: The prevalence of PI among older adults over 59 in China is 28·82%. Significant regional differences were observed in the duration of PA at different intensities. Older adults residing in more economically developed areas were more likely to engage in moderate-to-vigorous physical activity (MVPA) and exhibited longer sedentary behavior. Economic status and urban-rural disparities consistently emerged as direct influential factors across all intensity types. Chronic disease risks were significantly lower in active older adults compared to inactive ones. Lack of social guidance, family support, and personal inclination towards sedentary behavior were the main personalized factors affecting PA among older adults, and these factors could be relatively easily modified. CONCLUSIONS: Economic status, geography, and living areas (urban and rural) significantly influenced the distribution of physical activities in China. Particularly, economic status and living areas acted as direct factors. Older adults reaching the recommended standards for PA had significantly lower chronic disease risks, highlighting the importance of improving personalized factors which are crucial for promoting PA.

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BACKGROUND: The physical activity and health status of the students in China are not optimistic, there is a general lack of exercise volume and exercise intensity. Normal college students shoulder the future of China's education. Promoting their physical health is the basic requirement for cultivating teachers in the new era; Methods:Testing and recording 1123 male, 3266 female college students' physical fitness indicators in a normal college, the relationship between these indicators was mined by correlation analysis and Apriori, and the intelligent prediction models was constructed according to the mined knowledge; Results: There was no correlation between male 1000m running and vital capacity (P > 0.05), but it was correlated with vital capacity weight index (P < 0.05); Most indicators of women showed varying degrees of correlation. There are many association rules between female 50m sprint and standing long jump, sit-ups, and BMI. The introduction of vital capacity weight index slightly improved the accuracy of the 1000m run prediction model; The prediction model of female 50m sprint with standing long jump, sit-ups and BMI as inputs not only keeps the accuracy in a reasonable range, but also reduces the complexity and parameters; ConclusionsFor male students, the ostensibly paradoxical relationships between vital capacity and a 1000 meter run and between vital capacity and pull up were actually due to body shape; Body shape, lower limb explosive power, and core strength play key roles for female college students' speed quality; BMI, standing long jump and one minute sit-up can be used to predict the 50m sprint performance of general female college students.

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OBJECTIVES: Previous study has indicated that triiodothyronine (T3) facilitated cartilage degeneration in osteoarthritis (OA). This study aimed to investigate the effects of T3 on angiogenesis-related factor expression in human osteoblasts of OA subchondral bone. MATERIALS AND METHODS: The subchondral bone specimens were obtained from OA patients and healthy participants. The expressions of VEGF, HIF-1α, AKT, and phosphorylated AKT was detected by immunohistochemistry, Western blotting, and RT-qPCR in OA. Angiogenesis-related factor expression in OA osteoblasts was measured by treating different concentrations of T3. The hypoxia model and PX-478 (HIF-1α inhibitor) were employed to confirm the regulative role of HIF-1α for VEGF expression. The level of VEGF secretion was examined in osteoblasts supernatant using ELISA. RESULTS: Immunohistochemistry showed strong staining of VEGF and HIF-1α in OA subchondral bone. The expression of VEGF, HIF-1α, and p-AKT in OA osteoblasts was higher than that of normal osteoblasts at protein and mRNA levels. The physiological concentration of T3 (10-7 M) in OA osteoblasts up-regulated the expression of VEGF, HIF-1α, and p-AKT after 24 hr and 48 hr culture, while a higher dose of T3 displayed the adverse effects. Additionally, VEGF and p-AKT expression was down-regulated when PX-478 inhibited HIF-1α protein. CONCLUSION: Our results suggested that local T3 could effectively increase angiogenesis-related factor expression by PI3K/AKT signaling pathway, and HIF-1α regulated the VEGF expression in OA osteoblasts.

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AIMS: Previous study indicated that the increase of local bio-availability of 3'3'5-triiodothyronine (T3) influenced osteoarthritis (OA) initiation. We aimed to investigate the role of thyroid hormone receptors (THRs) signaling in OA osteoblasts. MATERIALS AND METHODS: THRs expression in OA was detected by immunohistochemistry, immunofluorescence, RT-qPCR and western blotting. These effects on the expression of angiogenesis-related factors were examined after THRα or THRß knockdown in OA osteoblasts. Fluorescence in situ hybridization was used to confirm the leading receptor for regulating angiogenesis-related factors. Co-culture model was utilized to observe the MMPs expression in chondrocytes after THRα knockdown in osteoblasts. The in vivo effects were also studied after intra-articular injection with THRα siRNA in OA model mice. Micro-CT and immunohistochemistry were employed to evaluate the changes of subchondral bone. KEY FINDINGS: THRs expression and nuclear translocation were upregulated in human OA osteoblasts. Immunohistochemistry showed that angiogenic activities were increased in OA subchondral bone of human and mice. VEGF, HIF-1α and IGF-1, these THR downstream genes were downregulated after THRα knockdown in OA osteoblasts. Fluorescence in situ hybridization further indicated that THRα signaling mainly regulated VEGF expression. Intra-articular injection with THRα siRNA reduced angiogenic activities in OA model mice subchondral bone and ameliorated cartilage degradation. Micro-CT analysis displayed that the aberrant subchondral bone formation in OA was promoted. SIGNIFICANCE: The microangiogenesis in subchondral bone may be partly attributed to abnormal THRα signaling in osteoblasts, and local inhibition of the THRα could be a potential target to treat OA.

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Osteoarthritis (OA) is involved in these pathophysiological changes of articular cartilage, subchondral bone and synovium. As a selective HDAC6 inhibitor, Ricolinostat (ACY-1215) has demonstrated chondroprotective effects in OA. However, its efficacy remains unclear in subchondral bone. In this study, we found that the mRNA and protein levels of HDAC6 were elevated in human OA osteoblasts in vitro. PI3K/AKT signaling pathway was suppressed with downregulation of VEGF expression in osteoblasts after ACY-1215 treatment. ACY-1215 promoted apoptosis of OA osteoblast in a concentration-dependent manner, and the expression of apoptosis-related proteins was also changed by activating caspase pathway. Moreover, western blotting showed decreased expression of MMP9 and MMP13 in IL-1ß-induced chondrocytes after co-culture with ACY-1215-stimulated osteoblasts. These data of immunohistochemistry and micro-CT from OA model mice also demonstrated the weak staining of MMPs in cartilage and prevention of aberrant subchondral bone formation after ACY-1215 injection. Therefore, high expression of HDAC6 in osteoblasts also contributed to the OA progression, and our study provided a new evidence that HDAC6 inhibitor may be a potential therapeutic drug for OA.

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