Archives of Medical Science最新文献

Introduction: Obesity and aging are established independent risk factors for osteoarthritis (OA). This study aimed to evaluate the correlation between the age-adjusted visceral adiposity index (AVAI) and OA.

Material and methods: This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) collected between 1999 and 2018. The correlation between AVAI and prevalence of OA was explored through receiver operating characteristic (ROC) regression, multivariate logistic regression, restricted cubic spline regression, and subgroup analysis.

Results: The study cohort comprised 20,628 participants, of whom 2,297 (11.1%) were diagnosed with OA. An increase in the quartile range of AVAI was correlated with a significant rise in the prevalence of OA (1.5% vs. 5.1% vs. 14.4% vs. 23.6%, p < 0.001). Logistic regression analysis demonstrated a significant positive correlation between AVAI and the risk of OA (OR = 1.14, 95% CI: 1.06, 1.23). Subgroup analyses indicated that this correlation was more pronounced in individuals aged over 60 years and those with diabetes. RCS regression analysis further identified a non-linear positive correlation, with an inflection point at -6.03. Finally, the area under the ROC curve (AUC) for AVAI was notably greater (AUC = 0.757, 95% CI: 0.747, 0.766) compared to traditional obesity indices.

Conclusions: This study is the first to demonstrate a significant positive correlation between the prevalence of OA and AVAI, with AVAI exhibiting superior diagnostic performance over traditional obesity indices in identifying OA.

Introduction: Congenital heart anomalies (CHAs) remain a significant global health issue for children, evidenced by persistent disparities in healthcare access across different socio-demographic index (SDI) regions and genders, despite slight decreases in prevalence.

Material and methods: This cross-sectional study used the Global Burden of Disease 2021 dataset to analyze CHAs in children aged 0-14 from 204 countries. Data analysis was performed using R software, incorporating global mapping, Joinpoint regression, and estimation of annual percent changes and rates, stratified by age, sex, and SDI.

Results: A total of 218,909,652 children, including 113,892,505 (52.03%) males and 105,017,147 (47.97%) females, were included in the analysis. From 1990 to 2021, the global prevalence of CHAs in children decreased by 4.294% (95% uncertainty interval [UI], -5.696-2.695%). Over three decades, CHA-associated deaths decreased from 497,979 (95% UI: 282,166-642,052) to 222,415 (95% UI: 181,359-275,182). The global mortality rate decreased from 28.633 (95% UI: 16.224-36.918) to 11.055 (95% UI: 9.014-13.678) per 100,000 population, while the prevalence rate changed from 377.257 cases per 100,000 in 1990 to 361.060 cases per 100,000 in 2021. Among the five SDI regions, the low SDI region had the highest CHA-associated mortality rate in 2021.

Conclusions: The study highlights the persistent global challenge of CHAs, particularly in low-SDI regions. It underscores the need for targeted public health interventions to reduce disparities and improve health outcomes globally.

Introduction: Obesity and weight fluctuations across adulthood are well-documented risk factors for cardiovascular diseases (CVDs), while serum uric acid has emerged as a potential metabolic intermediary influencing cardiovascular health (CVH). However, limited research has explored the life-stage-specific relationships between weight changes, uric acid levels, and CVH trajectories, particularly the mediating role of uric acid in these associations.

Material and methods: Multivariate linear regression was used to evaluate the associations between weight changes, uric acid levels, and CVH score patterns among 1,257 participants in NHANES cycles (2013-2018). Mediation analysis via bootstrap tests was conducted to investigate the role of uric acid in BMI-CVH relationships across life stages, with stratified analysis by sex.

Results: Obesity in early and middle adulthood was significantly associated with lower CVH scores in later adulthood. Weight changes exceeding 2.5 kg and stable obesity from middle to late adulthood were linked to increased cardiovascular risk. Serum uric acid levels were negatively associated with CVH scores and positively correlated with BMI and weight gain across all life stages. Uric acid mediated the relationship between BMI and CVH, with the mediating effect being most pronounced in early adulthood. Notably, this mediation effect showed gender differences, with a consistent effect across all stages in women but being significant only in late adulthood in men.

Conclusions: These findings underscore the complex interplay between weight, uric acid, and cardiovascular health. Maintaining a stable weight and effectively managing uric acid levels, with consideration of sex-specific differences, are critical strategies for improving cardiovascular outcomes across the lifespan.

Ensuring an adequate supply of essential micronutrients while preventing excessive intakes that could lead to adverse effects presents a challenge in the context of food supplement regulation, in the absence of harmonization in the European Union. This paper examines the scientific rationale and regulatory frameworks governing the definition of maximum allowable levels for vitamins and minerals in food supplements. Existing legislation, scientific literature, and institutional documents were considered, focusing on the different factors influencing the risk-benefit assessment, such as dietary habits, selection of the reference population, and the contribution of fortified and enriched foods to total nutrient intake. While a precautionary approach has been proposed to prevent potential risks linked to excessive intakes, too restrictive limits may undermine the nutritional role of supplementation. Future regulatory frameworks should integrate both safety and efficacy considerations, ensuring that supplements contribute meaningfully to micronutrient adequacy while preventing excessively high intake levels.

Introduction: Postpartum depression (PPD) is a severe emotional disorder affecting women worldwide, with significant impacts on maternal and infant health. Its genetic contributors and biological mechanisms are poorly understood. Identifying druggable genes and clarifying their causal roles may offer insights for developing more effective treatments.

Material and methods: We identified drug-related genes and screened gene expression quantitative trait loci (eQTL) from the eQTLGen consortium and genotype tissue expression (GTEx) v8 dataset, focusing on 13 brain tissues, along with Qi et al.'s meta-study on the cerebral cortex. Mendelian randomization (MR) analyses were used to investigate causal relationships between gene expression and PPD risk. Replication analyses in an independent PPD cohort validated initial findings, and meta-analysis combined MR results. Summary-data-based MR (SMR) and heterogeneity in dependent instruments (HEIDI) tests were also performed, followed by colocalization analyses to assess shared causal variants. Mediation analyses were conducted to explore how genetic effects may influence brain connectivity patterns.

Results: From 5,883 druggable genes, 37 showed potential causal links to PPD. Replication analyses confirmed 9 of these genes, with 4 remaining significant in meta-analysis. SMR and HEIDI analyses focused on CLCN7, which showed robust evidence for causal involvement in PPD. Colocalization analyses suggested shared causal variants, and mediation analyses revealed that CLCN7's genetic risk is partially mediated by left- to right-hemisphere visual network white-matter structural connectivity.

Conclusions: Our analysis identified CLCN7 as a potential causal factor in PPD, with its effect mediated through brain connectivity. These findings offer targets for future studies and therapeutic strategies for PPD.

Introduction: Plasma concentrations of cell-free DNA (cfDNA) serve as markers of overtraining or muscle injury. We examined whether nuclear (n) or mitochondrial (mt) cfDNA has potential as a marker of muscle burden or damage.

Material and methods: Ten healthy, physically active volunteers (6 females, aged 27.1 ±6.8 years) performed a downhill running test. Samples for cfnDNA and cell-free mitochondrial DNA (cfmtDNA) analysis were collected before, 30 min, 1 h, and 14 days after the downhill run. CfnDNA and cfmtDNA (two markers for each) were analyzed using qPCR.

Results: There was an extreme (~40-fold) increase in cfnDNA at the 30-min time-point against the baseline (p < 0.00001 for both markers), followed by a quick drop to baseline levels after 1 h after the end of the downhill run for all subjects. In contrast, plasma levels of cfmtDNA did not increase significantly (p = 0.27 and 0.12). It reflects the fact that in 6 subjects, the pattern was similar as for cfnDNA, but in 4 subjects a decrease of cfmtDNA concentration was observed at the 30-min time-point. These differences correlate with age, body mass index, and sex of the participants. Plasma cfnDNA significantly (p < 0.01 for all) correlated with concentrations of muscle damage markers such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LD), and chemokines MIP-1α and IP-10 (positive). No homogeneous correlation between cfmtDNA and biomarkers was detected.

Conclusions: Our study confirmed the extreme release and clearance of cfnDNA in physically active subjects after strenuous exercise. In contrast, the trajectory of cfmtDNA concentrations seems to have much higher inter-individual variability than cfnDNA concentrations.

Introduction: Oswestry Disability Index (ODI) and EuroQol-5D (EQ-5D) have been widely used to assess general health quality and function in clinical studies of patients with vertebral fractures. We aimed to investigate the associations of preoperative ODI and EQ-5D with long-term mortality in patients undergoing percutaneous vertebroplasty.

Material and methods: We retrospectively identified adult patients who had a single-level vertebral compression fracture and received percutaneous vertebroplasty between 2013 and 2020. Patients with traumatic fractures, burst fractures, and pathologic fractures, as well as those who had missing information on preoperative assessment of ODI and EQ-5D, were excluded. Survival status of the study patients was confirmed at the end of March 2021. The associations of preoperative ODI and EQ-5D with all-cause mortality were examined using Cox-proportional hazard models.

Results: A total of 167 patients were analyzed (mean age: 75.8 ±9.3 years, 25.7% male). There were 28 patients who died during a median follow-up duration of 2.1 years (63.6 per 1000 patient-years). Preoperative ODI was significantly associated with all-cause mortality after vertebroplasty (HR = 1.049, 95% CI: 1.008 to 1.092, p = 0.018). In contrast, preoperative EQ-5D was independently associated with a lower risk of all-cause mortality after the surgery (HR = 0.202, 95% CI: 0.043 to 0.936, p = 0.041).

Conclusions: Preoperative assessment of ODI (HR = 1.049, 95% CI: 1.008 to 1.092) and EQ-5D (HR = 0.202, 95% CI: 0.043 to 0.936) may help determine postoperative long-term mortality risk in this aging surgical population.