Archives of Medical Science最新文献

Introduction: Physical inactivity is a well-established risk factor for ischemic stroke, yet the global burden of ischemic stroke attributable to physical inactivity among older adults remains poorly understood. This study aimed to investigate the global burden of ischemic stroke attributable to physical inactivity among adults aged 55 and above from 1990 to 2021, focusing on socioeconomic status, regional variations, and temporal trends.

Material and methods: We calculated death and disability-adjusted life years (DALYs) on a global scale and across various Socio-demographic Index (SDI) regions. To analyze temporal trends, we employed joinpoint regression analysis. The total changes in disease burden were partitioned into three fundamental drivers: aging demographics, population expansion, and epidemiological trends. Additionally, the Bayesian age-period-cohort model was applied to forecast future trends.

Results: The global age-standardized death rate (ASDR) declined from 12.9 (95% UI: -2.3 to 28.6) in 1990 to 8.8 (95% UI: -2.7 to 21.2) in 2021, with an estimated annual percentage change (EAPC) of -1.53 (95% CI: -1.68 to -1.38). High SDI regions experienced the sharpest declines in both deaths and ASDR, while low and low-middle SDI regions showed slower progress. Joinpoint regression analysis revealed distinct temporal trends, with high SDI regions exhibiting the most substantial declines. Decomposition analysis highlighted the contributions of population growth and aging to increased disease burden, while epidemiological changes played a beneficial role in reducing the burden. Age and sex patterns revealed progressive increases in death and DALY rates with age, along with gender disparities, particularly in older age groups. The Bayesian age-period-cohort (BAPC) model projected a U-shaped trend in global ASDR for males and a consistent decline for females by 2050.

Conclusions: This research offers a thorough evaluation of the global impact of ischemic stroke due to physical inactivity in older adults between 1990 and 2021. The results underscore substantial inequalities in socioeconomic status and regional progress, noting particularly slow advancements in low and middle-income countries. The study highlights the necessity for focused interventions, enhanced healthcare accessibility, and robust stroke prevention initiatives to mitigate the global impact of ischemic stroke linked to physical inactivity. Future investigations should concentrate on examining the socio-economic, cultural, and policy-driven factors shaping these trends, thereby informing evidence-based approaches to alleviate the burden of ischemic stroke.

Introduction: Myocardial infarction (MI) is a leading cause of mortality, driven by inflammation and cardiac remodeling. While high-intensity interval training (HIIT) improves MI outcomes, its molecular mechanisms remain poorly defined, limiting therapeutic optimization. This study aimed to identify molecular targets and signaling pathways modulated by HIIT in MI, uncovering new therapeutic strategies for cardiovascular recovery.

Material and methods: Differential gene expression analysis of the GSE66360 dataset, comprising circulating endothelial cells from MI patients (n = 49) and healthy controls (n = 50), identified 481 DEGs. Cross-referencing with 717 HIIT-related genes from GeneCards revealed 39 overlapping genes. PPI and functional enrichment analyses highlighted seven hub genes: TNF, IL1B, MMP9, TLR4, ICAM1, TLR2, and CXCL1. These were validated by RT-qPCR in MI patients and controls (n = 20 each). MI was induced in rats (n = 8 per group), followed by an 8-week HIIT regimen. Infarct size, fibrosis, and protein expression were assessed using TTC staining, histology, and Western blot.

Results: We identified 481 DEGs in MI (351 upregulated, 130 downregulated; FDR-adjusted p < 0.05, |log2 fold change| > 1), with 39 overlapping HIIT-related genes. Seven hub genes (TNF, IL1B, MMP9, TLR4, ICAM1, TLR2, CXCL1) were upregulated in MI patients (p < 0.001, RT-qPCR). In MI rats, HIIT reduced infarct size by 32% (p < 0.01), decreased fibrosis and inflammatory cell infiltration (p < 0.05), and downregulated all seven hub genes (p < 0.05). Enrichment analyses linked these genes to TNF and TLR pathways, highlighting HIIT's anti-inflammatory effects.

Conclusions: HIIT protects the heart after MI by targeting inflammatory and remodeling pathways, providing a basis for precision cardiovascular therapy.

Introduction: Medication non-adherence (MNA) is a leading cause of graft loss and mortality in renal transplant recipients. Smartphone addiction (SPA) is associated with cognitive impairment and poor time management, but its relationship with MNA remains unclear. This is the first study to investigate the association between SPA and MNA in renal transplant recipients.

Material and methods: This cross-sectional study included 140 renal transplant recipients. SPA was assessed using the Smartphone Addiction Scale-Short Version (SAS-SV) and weekly screen time. MNA was measured using the Immunosuppressant Therapy Adherence Scale (ITAS), classifying adherence as perfect (12), acceptable (10-11), or poor (≤ 9). Univariate and multivariate logistic regression were performed to identify predictors of MNA.

Results: Patients with poor adherence had longer weekly screen time (27 ±10 h) than those with perfect (20 ±10 h) or acceptable adherence (21 ±11 h) (p < 0.001). The poor adherence group had a higher prevalence of SPA (66%) than the perfect (38%) and acceptable adherence groups (36%) (p = 0.020). In univariate analysis, higher SAS-SV scores (p = 0.006) and weekly screen time (p = 0.006) were associated with MNA. In multivariate analysis, only weekly screen time > 22 h remained an independent predictor (OR = 4.106, 95% CI: 1.366-12.336, p = 0.012), while SAS-SV scores lost significance.

Conclusions: Excessive smartphone use, particularly prolonged screen time, is independently associated with MNA in renal transplant recipients. Integrating screen time tracking into routine transplant care may help identify at-risk patients. Future studies should determine whether reducing screen exposure improves adherence.

Introduction: The aim of this study is to assess the effects of various exercise interventions of differing types and intensities (high-intensity aerobic training, moderate-intensity aerobic training, low-intensity aerobic training, high-intensity aerobic training combined with anaerobic training, high-intensity aerobic training combined with resistance training, moderate-intensity aerobic training combined with resistance training, mind-body exercises, and resistance training) on metabolic and cardiorespiratory function in children and adolescents with type 1 diabetes mellitus (T1DM).

Material and methods: Through systematic searches of databases such as PubMed, Embase, Cochrane, and Web of Science, randomized controlled trials (RCTs) were gathered to examine the effects of eight different types and intensities of exercise interventions on the metabolic and cardiorespiratory functions of children and adolescents with T1DM.

Results: A total of 19 RCTs involving 738 children and adolescents with T1DM were included. The network meta-analysis (NMA) results showed that high-intensity aerobic training combined with anaerobic training and high-intensity aerobic training significantly reduced the patients' lipid profile, including total cholesterol (TC) (MD = -1.92, 95% CI = (-2.36, -1.48)), low-density lipoprotein cholesterol (LDL-C) (MD = -1.18, 95% CI = (-1.94, -0.42)), and increased high-density lipoprotein cholesterol (HDL-C) (MD = 1.63, 95% CI = (1.21, 2.05)).

Conclusions: Based on NMA and surface under the cumulative ranking curve (SUCRA) rankings, it was concluded that high-intensity aerobic training combined with anaerobic training and high-intensity aerobic training can improve the metabolic and cardiorespiratory functions of children and adolescents with T1DM, although they did not show significant effects on hemoglobin A1c (HbA1c), blood glucose (BG), peak oxygen consumption (VO₂ peak), or triglycerides (TG).

Introduction: The study aimed to explore the causal association between genetically predicted sleep traits (chronotype, sleep duration, short sleep duration, long sleep duration, insomnia, daytime sleepiness, and sleep apnea syndrome) and diabetic nephropathy (DN).

Material and methods: A two-sample Mendelian randomization (MR) design was used to analyze summary data from genome-wide association studies of sleep traits and DN. The main analysis was conducted using the inverse variance weighted (IVW) method, and robustness was tested using the weighted median, weighted mode, and MR-Egger regression methods. Heterogeneity was detected using Cochran's Q-test, horizontal pleiotropy using the MR-Egger regression method, potential outliers using MR-PRESSO, and single-nucleotide polymorphisms driving the results using a leave-one-out analysis.

Results: The genetic prediction results indicated no statistically significant associations between the sleep traits and DN (all IVW p > 0.05). However, the weighted median analysis showed a possible causal association between long sleep and DN (OR < 0.01, 95% CI: 0-0.70, p = 0.04) and a borderline possible causal association between sleep apnea syndrome and DN (OR = 2.50, 95% CI: 0.99-6.35, p = 0.05). Cochran's Q-test indicated possible heterogeneity for the sleep duration analysis (p = 0.01), but no horizontal pleiotropy or outliers were detected (all p > 0.05).

Conclusions: This MR analysis suggested no causal associations between the sleep traits (chronotype, sleep duration, short sleep duration, long sleep duration, insomnia, daytime sleepiness, and sleep apnea syndrome) and DN. Further in-depth research is needed to examine the relationship between sleep and DN.

Introduction: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Ferroptosis, a regulated form of cell death driven by lipid peroxidation, has emerged as a potential therapeutic target. This study aimed to evaluate the expression levels of ferroptosis-associated genes GPX4, ACSL4, and BCAT2 in TNBC tissues and to investigate their potential as diagnostic or therapeutic biomarkers.

Material and methods: A total of 100 formalin-fixed paraffin-embedded (FFPE) breast tissue samples were analyzed, including 60 TNBC patient samples and 40 healthy controls. Gene expression levels of GPX4, ACSL4, and BCAT2 were determined using RT-qPCR. Statistical comparisons were conducted using the Mann-Whitney U test, and correlation analyses were performed using Spearman's test.

Results: The expression levels of GPX4, ACSL4, and BCAT2 were significantly lower in the TNBC group compared to controls (p = 0.0001 for all genes). Strong positive correlations were observed among the three genes, with BCAT2 showing the highest correlation with both GPX4 (R = 0.636) and ACSL4 (R = 0.683). Additionally, BCAT2 expression negatively correlated with tumor diameter and Ki-67 index.

Conclusions: The significant downregulation and strong positive correlation of GPX4, ACSL4, and BCAT2 in TNBC tissues suggest coordinated suppression of ferroptosis. These findings highlight the potential of targeting ferroptosis as a novel therapeutic strategy in TNBC and propose these genes as candidate biomarkers for diagnosis and treatment response.