Meng Zhao

Rheumatoid arthritis (RA) is a leading cause of disability worldwide. Although global assessments of RA have been reported, age-specific estimates focusing on middle-aged adults [middle-aged adults (MAA); 40-59 years] remain limited. To quantify the global, regional, and temporal burden of RA among MAA from 1990 to 2021 and project age-standardized trends through 2050. A population-based descriptive epidemiological study using Global Burden of Disease (GBD) 2021 estimates. GBD 2021 data (1990-2021) were used to estimate age-standardized incidence (ASIR), prevalence (ASPR), mortality (ASMR), and disability-adjusted life-year rates (ASDR) per 100,000 population among MAA. Temporal trends were assessed using joinpoint regression and expressed as the average annual percentage change (AAPC). Projections to 2050 were generated using a Bayesian age-period-cohort model. Burden patterns were summarized across sociodemographic index quintiles and 21 GBD regions. In 2021, the global ASIR, ASPR, ASMR, and ASDR among MAA were 19.53, 368.73, 0.19, and 56.74 per 100,000 population, respectively. From 1990 to 2021, ASIR and ASPR increased (AAPC = 0.24% and 0.43%), ASMR decreased (AAPC = -1.70%), and ASDR showed minimal net change (AAPC = 0.05%). Substantial variation was observed across SDI quintiles and GBD regions; SDI was positively correlated with ASIR and ASPR and negatively correlated with ASMR. Projections to 2050 indicated an ASIR of 19.22, an ASPR of 367.47, an ASMR of 0.111, and an ASDR of 52.18 per 100,000, with widening credible intervals over time. Between 1990 and 2021, the RA burden among MAA was characterized by increasing ASIR and ASPR, declining ASMR, and relatively stable ASDR. Projections suggest that ASIR and ASPR will remain near recent levels, whereas ASMR and ASDR will show lower median values over time.

Background: Based on the results of existing observational studies, it can be found that the association between serum vitamin D levels and the risk of Sjogren’s syndrome (SS) in humans is still controversial. Based on this situation, this study aimed to assess the causal relationship between serum vitamin D levels and SS by using the Mendelian randomization (MR) approach. Methods: In this study, genome-wide association studies (GWAS) summary statistics on serum vitamin D levels [sample size = 417,580 (UK Biobank)] and SS [sample size = 416,757 (cases = 2495, controls = 414,262) (FinnGen)] were used. The bi-directional MR analysis was then used to assess possible causal relationships. The major analysis method of MR was performed using inverse-variance weighted (IVW), supplemented by MR-Egger and the weighted median approaches. In addition, sensitivity analyses were used to ensure the stability of the results, including Cochran’s Q test, MR-PRESSO, MR-Egger intercept test, and the leave-one-out test. Results: The MR suggested that no significant causal effects of serum 25(OH)D levels on SS risks were observed [odds ratio (OR) = 0.9824; 95% confidence interval (CI) = 0.7130 to 1.3538; P = 0.9137]. Similarly, no evidence supported the causal effects of SS on serum vitamin D levels (β: 0.0076, 95% CI: − 0.0031 to 0.0183; P = 0.1640). Conclusion: This study found no obvious evidence that serum vitamin D level is causally associated with SS risks or vice versa. We call for larger sample size studies to further unravel the potential causal relationship and the exact mechanism.

Estimation of the skeleton-protective effects of Ca in Cd-induced bone damage is helpful in the assessment of Cd health risk. The aim of this study was to identify whether Ca supplementation during exposure to different population-relevant doses of Cd can prevent Cd-induced bone damage under the tolerable upper intake level of Ca supplementation. Young female Sprague-Dawley rats were given different population-relevant doses of Cd (1, 5, and 50 mg Cd/kg diet) and Ca supplementation (0.4% Ca supplementation) intervention. Ca supplementation significantly decreased Cd-induced bone microstructure damage, increased bone biomechanics (p < 0.05), serum bone formation marker level (p < 0.05) and expression of osteogenic gene markers exposure to the 5 and 50 mg Cd/kg diets. However, it had no impact on these indicators under the 1 mg Cd/kg diets, with the exception of expression of osteogenic marker genes. Ca supplementation significantly decreased serum Klotho level (p < 0.05), and fibroblast growth factor 23/Klotho-associated gene expression in the kidney and bone showed significant changes. In conclusion, Ca supplementation has a positive effect on bone formation and bone quality against the damaging impact of Cd, especially with exposure to the 5 mg and 50 mg Cd/kg diet, which may be related to its impact on the fibroblast growth factor 23/Klotho axis.