Peripheral arterial disease (PAD) is a common cardiovascular disease that it is an important reason for the decline of patients’ quality of life and the increase of family economic burden. To systematically evaluate the association between environmental lead exposure and peripheral arterial disease (PAD) and to characterize the global distribution of PAD disease burden, while exploring differences among regions with varying socioeconomic development. Using data from the National Health and Nutrition Examination Survey (NHANES), the Global Burden of Disease (GBD) database, and genome-wide association studies (GWAS), we employed multivariable logistic regression to examine the link between lead exposure and PAD. Mendelian randomization (MR) was used to infer causality, and we analyzed PAD disease burden trends across countries of differing income levels. The burden on PAD patients worldwide shows a downward trend. In high SDI and high middle SDI countries, the burden of PAD gradually decreases, while in low middle SDI and low SDI countries, the burden of PAD gradually decreases. After adjusting for potential confounders, a significant dose-response relationship was observed between blood lead levels and PAD risk (OR = 1.04, 95% CI: 1.00-1.09). This association was more pronounced among males (OR = 1.07, 95% CI: 1.05–1.09), individuals with higher education (OR = 1.24, 95% CI: 1.16–1.32), and patients with hypertension (OR = 1.07, 95% CI: 1.05–1.09). MR analysis supported a causal link between lead exposure and PAD. Global trend analysis indicated that PAD burden is declining in high-income countries but rising in low-income regions, highlighting significant health inequities. Environmental lead exposure is significantly associated with increased PAD risk, with notable differences in population susceptibility. These findings underscore the necessity of environmental exposure control and tailored prevention strategies to enhance cardiovascular health worldwide.

Background: Patients with systemic lupus erythematosus (SLE) suffer from a high incidence of premature ovarian failure, which might be due to cyclophosphamide gonadal toxicity, immune abnormalities, or other reasons. This study aimed to investigate whether the transplantation of human umbilical cord mesenchymal stem cells (HUC‐MSCs) can improve ovarian reserve function in lupus mice.Methods: We used MRL/lpr mice to observe changes in ovarian structure and secretory function in SLE. Lupus mice and controls were injected with HUC‐MSCs at Weeks 12 and 16. We detected serum concentrations of the sex hormones estradiol (E2), follicle‐stimulating hormone (FSH), and anti‐Müllerian hormone (AMH), using enzyme‐linked immunosorbent assays. Hematoxylin and eosin staining showed ovarian tissue structure and enabled the counting of follicles. Hepatocyte growth factor (HGF) and insulin‐like growth factor 1 (IGF‐1) expression in ovarian tissue was observed by immunohistochemistry.Results: Ovarian function in lupus mice was abnormal, as indicated by decreased serum E2 and AMH concentrations, and increased FSH concentrations. HUC‐MSC transplantation caused significant upregulation of serum E2 and AMH and downregulation of FSH (all p < 0.05). Ovarian structure improved and the follicle number increased after HUC‐MSC transplantation. Multiple infusions of HUC‐MSCs at Weeks 12 and 16 resulted in a significantly higher number of primordial follicles than infusions of HUC‐MSCs at only Week 12 (p < 0.05). Immunohistochemistry showed that IGF‐1 and HGF expression increased after HUC‐MSC transplantation, but this was not significant.Conclusions: HUC‐MSCs transplantation restores disturbed hormone secretion and folliculogenesis in lupus mice. HUC‐MSC transplantation should be repeated for the best treatment effect.

Rheumatoid arthritis (RA) is a chronic inflammatory disease requiring early diagnosis and treatment to achieve sustained clinical remission. Achieving a state of remission is associated with favorable outcomes. However, predictive factors for Boolean2.0 remission in RA patients are limited. This retrospective observational study analyzed data from RA patients enrolled in a smart system of disease management group (SSDM) between January 2014 and December 2023. Demographic and clinical characteristics were compared between patients who achieved Boolean2.0 remission and those who did not. Univariate and multivariate logistic regression analyses were performed to identify predictive factors associated with Boolean2.0 remission. Among 5004 patients enrolled for analysis, 541 (10.8%) achieved Boolean2.0 remission. The median (IQR) age at diagnosis of the patients was 51.00 (42.00, 60.00) years, with the majority being female (3978, 79.5%). The median (IQR) disease duration was 26.00 (3.00, 89.00) months. Logistic regression analyses revealed that the likelihood of achieving Boolean2.0 remission was greater in patients who were younger (P = 0.008), had a shorter disease duration (P < 0.001), a lower number of tender joints (P < 0.001), and were prescribed methotrexate (P = 0.012) and leflunomide (P = 0.001). Younger age, shorter disease duration, lower count of tender joints, and treatment with methotrexate and leflunomide were associated with increased likelihood of achieving Boolean2.0 remission. These findings can guide clinicians in identifying high-risk patients and optimizing treatment strategies.

Introduction: The clinical heterogeneity of non-alcoholic fatty liver disease (NAFLD) across BMI strata warrants further investigation. This study examined the cross-sectional association between lean NAFLD and carotid plaque (CP) in a Chinese health check-up population, and the prospective association between lean NAFLD and incident diabetes in a Japanese cohort. Methods: The study comprised a Chinese cross-sectional analysis ( n = 12,283) and a Japanese prospective cohort analysis ( n = 14,271). In both analyses, participants were classified into four groups: G1 (BMI ≤ 23 kg/m ² , without NAFLD), G2 (BMI > 23 kg/m ² , without NAFLD), G3 (BMI ≤ 23 kg/m ² , with NAFLD; i.e., lean NAFLD), and G4 (BMI > 23 kg/m ² , with NAFLD; i.e., non-lean NAFLD). Multivariable logistic regression was used to examine the prevalence of CP and of hypoechoic or heteroechoic carotid plaques, and Cox proportional hazards models were used to estimate incident diabetes risk. Additive interaction was assessed using the relative excess risk due to interaction (RERI), attributable proportion (AP), and synergy index (SI). Results: In the cross-sectional analysis, G3 (OR = 1.596, 95% CI 1.282–1.983, p < 0.001) and G4 (OR = 1.461, 95% CI 1.276–1.672, p < 0.001) were significantly associated with higher odds of CP relative to G1. Among participants with CP, the proportion of hypoechoic or heteroechoic carotid plaques was highest in G4 and was significantly higher than that in G3 (adjusted p = 0.018). In the prospective analysis, both G3 (HR = 5.637, 95% CI 3.626–8.762) and G4 (HR = 8.133, 95% CI 5.970–11.078) showed significantly elevated diabetes risk versus G1 ( p < 0.001); risk did not differ significantly between G3 and G4 ( p > 0.05). Additive interaction analysis showed no significant interaction between BMI and NAFLD for CP ( p > 0.05). Conclusion: No statistically significant difference was detected between lean NAFLD and non-lean NAFLD regarding their associations with carotid plaque prevalence and incident diabetes risk. Notably, this non-significant finding does not indicate equivalence of risk magnitudes between the two groups, and the relatively small number of diabetes events in the lean NAFLD group may have limited the statistical power to detect potential group differences.