chronic conditions: heart problems, high blood pressure, stroke, diabetes, asthma, osteoarthritis (OA), total hip replacement (THR), total knee replacement (TKR), anxiety, depression, and dementia. Only male participants from the former cricketer and general populations were included in analysis. Standardized mortality ratios (SMRs) and their 95% confidence intervals (CI) were used to compare prevalences of chronic condition outcomes in former cricketers aged 50 and over to a general population sample from the English Longitudinal Study of Ageing (ELSA). Both the former cricketer sample and general population were standardized by gender, age, and BMI for analysis. Results: 113 former elite cricketers were included from the cricketer sample, with a mean age of 65.1 (SD 9.1) and mean BMI of 27.9 (SD 4.0), and 4496 participants were included from the general population sample, with a mean age of 64.2 (SD 9.6) and mean BMI of 27.6 (SD 3.8). The prevalence of heart problems was significantly reduced in the former cricketers compared to the general population (ELSA) with an SMR of 0.55 (CI 0.33-0.91) (see table). OA, THR, and TKR were significantly increased in the former cricketers compared to the general population, with SMRs of 3.64 (CI 2.81-4.71), 3.99 (CI 2.21-7.20), and 3.84 (CI 1.92-7.68), respectively. The SMRs for anxiety and depression were also significantly increased in former cricketers compared to the general population, at 3.95 (CI 2.34-6.67) and 2.22 (CI 1.20-4.14), respectively. Conclusions: Musculoskeletal and mental health outcomes measured in this study were significantly increased in the former cricketers compared to the general population (ELSA). Cardiovascular conditions in the former cricketers were either significantly decreased (heart problems) or not significantly different (high blood pressure, stroke) compared to the general population. This study presents the first data of its kind amongst former elite cricketers, which will be important to enable a balanced assessment of the long-term health impacts of cricket and also to identify strategies to prevent and mitigate negative outcomes for future cricketers.
Purpose: MiRNA-381 is known to regulate osteoarthritic cartilage degeneration in our previous study, but its target remains unclear. The aim of this study is to identify histone deacetylase 4 (HDAC4), an inhibitor of chondrocyte hypertrophy, as a target of miRNA-381. Methods: The long bone of forearm in mouse embryo served as an in vivo model of chondrogenesis and hypertrophy. The expression of miRNA-381was determined by in situ hybridization, while HDAC4 and MMP13 levels were detected by immunohistochemistry.SW1353 chondrocyte-like cells and primary mouse chondrocytes (PMCs) was transfected with miRNA-381 mimic or miRNA-381 inhibitor in vitro. HDAC4 siRNA was used to determine its function in chondrocyte differentiation and hypertrophy. Direct interaction between miR-381 and putative site in the 3 0-untranslated region (3 0-UTR) of HDAC4 messenger RNA was validated by luciferase reporter assay. Results: MiRNA-381, RUNX2 and MMP13 were mainly expressed in hypertrophic chondrocytes, while HDAC4 showed a high expression in pre-hypertrophicchondrocytes and decreased apparently in hypertrophic zone. Overexpression of miRNA-381 suppressed the activity of a reporter construct containing the 3 0-UTR, decreased HDAC4 expression and increased acetylated-Histone H3, RUNX2 and MMP13. Down-regulaiton of HDAC4 using siRNA significantly increased RUNX2 expression. Conclusions: MiRNA381 epigenetically regulates chondrocyte hypertrophy and degeneration by directly targeting HDAC4.
Purpose: The pro-inflammatory cytokine interleukin-1beta (IL-1b) plays critical roles in pathogenesis of osteoarthritis (OA). Tormentic acid (TA), a triterpene isolated from Rosa rugose, has anti-inflammatory activity. However, the anti-inflammatory effect of TA on OA is still unclear. So, in the present study, we examined the effect of TA on IL-1binduced inflammatory response in primary human OA chondrocytes. Methods: Chondrocytes were isolated from patients. MTT assay was used to detect cell viability. The MMP-3, MMP-13, COX-2 and iNOS mRNA expression were evaluated via RT-PCR. The protein expression of MMP-3, MMP-13, iNOS, COX2, NF-kB p65 and NF-kB p65 were detected by western blot.The nitrite levels in the culture medium were determined by Griess reaction. Statistical significance was assessed by the one-way analysis of variance (ANOVA). Results: Our results demonstrated that TA significantly decreased the IL-1b-stimulated the expression of matrix metalloproteinase-3 (MMP-3) and MMP-13. It also inhibited the IL-1b-induced the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the production of nitric oxide (NO)and prostaglandin E2(PGE2) in human OA chondrocytes. Furthermore, TA greatly inhibited the IL-1binduced NF-kB activation. Conclusions: In conclusion, this study is first to demonstrate the antiinflammatory activity of TA in human OA chondrocytes. TA significantly inhibits the IL-1b-induced inflammatory response by suppressing the NF-kB signaling pathway. Thus, TA may be a potential agent in the treatment of OA.
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