Low back pain (LBP) is a common condition and the leading cause of disability worldwide. Medical students may be at higher risk due to prolonged sitting and stress. The aim of this study was to examine the prevalence of LBP and disability among Polish medical students and identify associated risk factors. In this study, 533 medical students, predominantly female (66.4%), with a median age of 22, were surveyed via an online questionnaire. The survey used the Oswestry Disability Index (ODI) and Patient Health Questionnaire (PHQ-9) to evaluate LBP and depression symptoms. Demographic data and information on smoking, exercise, sitting duration, spine posture, past and present LBP, pain duration, intensity, and analgesic use were also collected. Point prevalence LBP was 70.95%, while 78.26% of participants reported past history of LBP. The median LBP intensity measured with the Numeric Rating Scale (NRS) was 3, and the median ODI score was 10%. Overall, female medical students suffered more from LBP than males (66.4% vs. 33.6%). The following LBP risk factors were identified in the studied group: past episodes of LBP (OR = 2.92), sitting 8 h/day (OR = 2.44), as well as 10 h or more (OR = 2.95), moderate and severe depression symptoms (OR = 2.51, OR = 7.33 respectively). Prevalence of low back pain among medical students in the studied group is high, resulting in mild disability, with females experiencing more severe symptoms than males. Past LBP episodes, sitting 8 h or more, and depression symptoms are independent risk factors for development of LBP among Polish medical students.
Personalized medicine in inflammatory bowel disease (IBD) aims to achieve maximum effectiveness through rapid induction and maintenance of remission. To achieve this goal, reliable predictors of disease course are needed. The aim of this study was to identify early markers of IBD's poor course understood as the need for anti-tumor necrosis factor (anti-TNF-α) treatment. We analyzed the clinical, laboratory, radiological, and endoscopic data of children with IBD. These parameters were assessed at the time of diagnosis (T0) and 8-12 weeks (T1) after the start of induction therapy. The results of patients who did not require anti-TNF-α treatment were compared to children who needed such treatment during the 2-year observation time. 58.14% of patients with Crohn's disease (CD) and 31.71% of patients with ulcerative colitis (UC) required biological therapy. Patients with CD and UC receiving biological therapy, compared with those without, differed in selected clinical and laboratory parameters both at T0 and T1. In multivariate analysis, the risk of anti-TNF-α therapy in patients with CD was associated with the lack of normalization of mean corpuscular volume (MCV) and Pediatric Crohn's Disease Activity Index (PCDAI). In patients with UC, higher albumin levels reduced this risk. In children with IBD, disease activity and concentrations of selected biochemical parameters assessed within 3 months after diagnosis may be helpful in predicting a poor outcome of CD and UC.
Single-bundle autologous hamstring tendon reconstruction is a surgical procedure used primarily in orthopedics. The aim of the study was to investigate the impact of using autologous hamstring tendon single-bundle restoration in conjunction with braided threads on both joint stability and clinical efficacy in patients suffering from posterior cruciate ligament (PCL) rupture. In total, 106 patients diagnosed with PCL rupture were randomly assigned to the control group and study group, each group consisting of 53 patients. The control group received autologous hamstring tendon single-bundle reconstruction, whereas the study group received autologous hamstring tendon single-bundle reconstruction together with braided thread treatment. The comparative rates of treatment success and satisfaction, complication occurrence, pre-and post-surgery joint activity indicators, gait parameters, knee joint function, and joint stability were assessed. The study group showed a significantly higher rate of excellent and good treatment outcomes compared to the control group (p < 0.05). Twelve months after surgery, the study group showed significantly higher joint activity index, stride length, stride speed, and Rasmussen score compared to the control group. The single-bundle reconstruction combined with braided thread has good clinical efficacy in patients with PCL rupture and more effectively improves the patient's joint stability.
This state-of-the-art review surveys the rapidly advancing field of triglyceride-lowering therapies as of 2025, positioning hypertriglyceridemia (HTG) as both a residual driver of atherosclerotic cardiovascular disease (ASCVD) and a key precipitant of acute pancreatitis. After outlining the pathophysiological role of elevated triglycerides - via remnant lipoproteins, inflammation and endothelial dysfunction, often within the lipid triad of low high-density lipoprotein-cholesterol (HDL-C) and small, dense low-density lipoprotein (LDL) - we evaluate established and emerging pharmacologic options. Fenofibrate, a PPAR-α activator, remains a cornerstone for mixed dyslipidemia, improving micro- and macrovascular outcomes in diabetes. Purified eicosapentaenoic acid (icosapent ethyl) is highlighted for its robust reduction of major adverse cardiovascular events despite neutral triglyceride thresholds, albeit with a modest increase in atrial fibrillation risk. Novel agents targeting apolipoprotein C-III (volanesorsen, olezarsen, plozasiran) achieve profound triglyceride declines and substantially mitigate pancreatitis in familial chylomicronemia syndrome (FCS), while angiopoietin-like 3 (ANGPTL3) inhibitors and fibroblast growth factor 21 (FGF21) agonists demonstrate early promise in broad atherogenic-lipid reduction and metabolic modulation. The paper emphasizes the importance of genetic testing to differentiate FCS from multifactorial chylomicronemia syndrome, guiding personalized therapy. Current guidelines endorse icosapent ethyl and fenofibrate for high-risk HTG, with apoC-III inhibitors poised to become first-line for FCS as access improves. Ongoing trials of ANGPTL3 inhibitors, FGF21 agonists and gene-editing approaches may soon redefine lifelong lipid management.
We aimed to estimate the incidence of depression among women of childbearing age between 1990 and 2019 in terms of age, sex, country, and Socio-Demographic Index (SDI). This study analyzed trends in age-standardized incidence rates (ASIR) and disability-adjusted life years (DALYs) using data from the Global Burden of Disease Study. We calculated the estimated annual percentage change (EAPC) and its corresponding 95% confidence interval (CI). From 1990 to 2019, the ASIR (per 100,000) and age-standardized DALY rate (per 100,000) of depression in women of childbearing age showed a decreasing trend, with EAPC values of -0.53 and -0.44, respectively. Singapore's ASIR and Cuba's age-standardized DALY rate had the lowest EAPC (-2.24 and -2.11). Among the 21 geographical regions, the ASIR and DALY in Central Latin America had the highest EAPC (EAPC of 0.74 and 0.66, respectively), while East Asia had the lowest EAPC (-1.79 and -1.45, respectively). When looking at the changes in ASIR and age-standardized DALY rates from a national perspective, Mexico, Spain, and Germany had the largest increases in ASIR and age-standardized DALY rates. The EAPCs of depression ASIR in women of childbearing age were 1.55, 1.46, and 1.17, respectively, and the EAPCs of depression age-standardized DALY rates in women of childbearing age were 1.40, 1.29, and 1.01, respectively. From 1990 to 2019, there was a consistent downward trend in the burden of depression in women of childbearing age globally. However, certain countries and regions such as Central Latin America (including Mexico) experienced an upward trend in ASIR and age-standardized DALY rates.
Cuproptosis is an emerging form of programmed cell death that has been implicated in tumor progression. Nevertheless, the relationship between cuproptosis and the metastatic process in colorectal cancer (CRC) remains obscure, as are the underlying molecular mechanisms that drive CRC progression in this process. Bioinformatics, quantitative reverse transcription polymerase chain reaction (qRT-PCR), immunofluorescence (IF), and Western blot (WB) were leveraged to analyze the expression levels of RBM24 in CRC. Cell Counting Kit-8 (CCK-8) assay, Transwell, and WB assays were conducted to determine the cell proliferation, migration, and invasive potential, alongside the expression analysis of metastasis-related proteins. Intracellular Cu2+ levels were quantified using a Copper Assay Kit. Additionally, the expression of mitogen-activated protein kinase (MAPK) pathway and cuproptosis-related proteins were probed via WB. RBM24 was under-expressed in CRC, and its forced expression inhibited the metastatic abilities of CRC cells, including migration, invasion, and epithelial-mesenchymal transition (EMT). The use of a MAPK pathway inhibitor could temper the pro-metastatic effects associated with low RBM24 levels. At the molecular level, the combination of copper ionophores with copper ions (Es-Cu) upregulated RBM24, leading to the inhibition of CRC cell spread. The effects of cuproptosis on CRC cells were abolished by knocking down RBM24. Elevated levels of cuproptosis-induced cell death disrupt the MAPK signaling cascade, thus suppressing the metastasis of CRC. This discovery sheds new light on the potential application of cuproptosis in oncological treatments.
Bladder cancer is a highly recurrent malignancy and frequently shows drug resistance. Although gemcitabine initially works well for most patients, the majority of treated patients progressively generate resistance after multiple rounds of therapy, eventually leading to tumor recurrence. Recent studies suggest that a small subpopulation of cancer cells with stem cell-like properties - cancer stem cells - may be responsible for chemoresistance and tumor recurrence. Circular RNAs (circRNAs) are novel non-coding RNAs with great potential as cancer therapy. The levels of circRNA_103809 in bladder cancer cells and a normal urothelial cell line were measured by quantitative polymerase chain reaction (qPCR). Bladder cancer cells were depleted of circRNA_103809, then in vitro and in vivo cell growth, migration, invasion, sphere formation ability, and resistance to gemcitabine were analyzed. The biomarkers of cell migration, invasion, and stemness were detected by western blotting assay. The interaction between miR-516a with circRNA_103809 or FBXL18 3'UTR was detected by luciferase reporter gene assay and an RNA pulldown experiment. Depletion of circRNA_103809 significantly suppressed the viability of bladder cancer cells, reduced cell migration and invasion, increased sensitivity to gemcitabine, and repressed cancer cell stemness. Further investigation of the molecular mechanism revealed that circRNA_103809 interacted with miR-516a to modulate the expression of FBXL18 in bladder cancer cells. CircRNA_103809 acts as a potential promoter of bladder cancer through sponging miR-516a to upregulate FBXL18. Our findings identify circRNA_103809 as a potential target for bladder cancer therapy.
Diabetes mellitus (DM) is associated with increased mortality in hospitalized adults. However, data regarding the impact of DM on long-term mortality after discharge in very old patients are scarce. This prospective study assessed 3-year post-discharge mortality and its predictive factors in older patients, focusing on possible differences between patients with and without DM. Medical history, chronic medication use, clinical and laboratory characteristics, Charlson Comorbidity Index (CCI), 5-item Fried Frailty Score (FFS), Clinical Frailty Scale (CFS), Barthel Index (BI), and Katz Index were recorded on admission. A total of 815 older adults (46.0% males) with a median age of 83.0 years (IQR: 77.0-88.0) were included in the study. The 3-year mortality rate was 54.9% in patients with DM (n = 368) and 60.2% in patients without DM (n = 447, p = 0.13 between groups). In multivariate logistic analysis, nursing home residency, higher CCI, higher CFS, higher FFS, lower BI, the total number of days of hospitalization in the past year, and hospital-acquired infections were independently associated with the 3-year mortality in both groups. In individuals with DM, lower body mass index (BMI) and elevated urine albumin-to-creatinine ratio (UACR) were identified as additional independent predictors of 3-year mortality. A high post-discharge mortality rate was observed in very old patients. DM was not identified as an independent factor of post-discharge mortality. Assessment of frailty and disability in very old patients is important for predicting long-term post-discharge mortality. Additionally, in patients with DM, evaluating BMI and UACR may aid in better prediction of 3-year mortality.
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. 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. 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. 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.
The role of mothers has long been the subject of social stereotyping and debate. Psychological and sociological research suggests that women approach this role with a complex ability to multitask, often prioritising family care over career development. For the present study, an anonymous online questionnaire was developed to collect data from 534 female doctors who are mothers ('mother doctors'). The 32-item questionnaire focused on the relationship between their careers and family life, covering demographic information, family configuration, availability of home help, division of household responsibilities and the impact of these factors on their professional life. The study found that the majority of female doctors surveyed (51.7%) stated unequivocally that motherhood had a significant impact on their approach to patients, with 30.7% indicating a moderate impact. The most commonly cited changes at work related to motherhood were a greater understanding of the needs of patients, especially mothers and children (79.1%), as well as increased empathy (59.0%) and changes in communication style (54.7%) with patients. Motherhood represents a profoundly transformative experience in the professional lives of women doctors, the impact of which goes far beyond stereotypical limitations. Accumulating evidence suggests that mother doctors not only become more organised and resilient to stress, but also develop leadership skills that can contribute to the transformation of the healthcare system in Poland. Childcare challenges are one of the most significant barriers to academic success for mother doctors.
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. 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. 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. 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.
Meningioma, a prevalent intracranial tumor, presents diagnostic and therapeutic challenges due to its heterogeneous nature. Metabolic profiling has emerged as a promising approach to elucidate its underlying molecular mechanisms and discover potential biomarkers. This study employed bidirectional Mendelian randomization (MR) analysis to investigate the causal relationship between plasma metabolites and meningioma risk. Genetic instruments were used as surrogates for both plasma metabolites and meningioma, allowing MR analysis in both directions to assess the impact of metabolites on meningioma risk and vice versa. This study encompassed data on 1400 plasma metabolites and 314,708 participants (1316 individuals diagnosed with meningioma and 313,392 individuals without meningioma). Initially, 46 plasma metabolites/metabolite ratios were found to be associated with meningioma risk (p < 0.05), with 23 associated with a decreased risk and 23 associated with an increased risk of meningioma. Furthermore, the identified relationships between the 46 plasma metabolites/metabolite ratios and meningioma showed no significant horizontal pleiotropy (p > 0.05), suggesting that the results are not influenced by other confounding factors. Reverse MR analysis revealed that meningioma has no significant impact on the levels of 24 plasma metabolites/metabolite ratios, and is unaffected by confounding factors. In addition, the identified plasma metabolites influence the occurrence of meningioma through nine metabolic pathways. The findings of this bidirectional MR study indicate that 24 plasma metabolites/metabolite ratios lead to a significantly increased/decreased risk of meningioma, suggesting that the plasma metabolite profile characteristics serve as important serological tools for the early diagnosis of meningioma.
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. 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. 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. 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.
Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in Poland. Lipoprotein(a) [Lp(a)] constitutes an independent, causal risk factor for ASCVD and aortic valve stenosis. Elevated Lp(a) is found in approximately 20% of the Polish population. Lp(a) measurements have been recommended in all adult patients to improve cardiovascular risk stratification. As the testing rate remains insufficient, there is a need to facilitate the incorporation of Lp(a) into routine patient care. This clinically oriented review outlines (i) up-to-date evidence on the role of Lp(a) in cardiovascular diseases, (ii) recent real-world data on the characteristics of Polish patients with elevated Lp(a), and (iii) strategies for Lp(a) testing and management in light of the current national recommendations and the latest 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidemias.
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.
Given insulin resistance's (IR) critical role in metabolic pathophysiology, this study aims to identify optimal coffee consumption patterns by timing and dose to improve population health. Multivariate logistic regression and restricted cubic splines assessed associations between coffee timing, dosage, and IR (measured by estimated glucose disposal rate) from NHANES data (1999-2018). Interaction and subgroup analyses explored variations across population segments. We analysed 21,138 participants, of whom 46.79% were non-consumers. Among consumers, 76% primarily drank coffee in the morning. Morning consumption at the lowest quartile (Q1) showed significant improvement in IR (odds ratio [OR] = 1.37, 95% confidence interval [CI]: 1.16-1.62), although this benefit diminished with higher consumption levels (p < 0.05). While the "all-day" pattern overall showed a non-significant trend toward improved insulin resistance (OR = 1.20, 95% CI: 0.83-1.73), higher consumption within this pattern (Q3: OR = 1.46, 95% CI: 1.13-1.89; Q4: OR = 1.34, 95% CI: 1.11-1.63) proved significantly more beneficial than lower intake. Comparative analysis revealed that morning consumption tended to be more advantageous for low-to-moderate intake (Q1-Q2), whereas all-day distribution showed potential benefits at higher consumption levels (Q3-Q4). The observed benefits were primarily associated with caffeinated coffee, attenuated by sugar addition, and varied across subgroups based on age, sex, and comorbidities. Both morning and all-day coffee intake improve IR. For moderate consumption (1-2 cups/day), morning intake provides optimal improvement in insulin sensitivity. For higher intake (≥ 3 cups/day), distributed consumption is more effective. These findings support chrono-nutrition principles for optimising metabolic health through coffee consumption.
β-thalassemia is a genetic disorder characterized by a quantitative defect in β-globin synthesis caused by genetic and epigenetic alterations. However, the expression patterns of long non-coding RNAs (LncRNAs) and their relationship with genes and proteins involved in iron metabolism and erythropoiesis remain largely unknown. We aimed to investigate the expression of LncRNAs and their correlation with iron and erythropoiesis regulatory proteins in patients with transfusion-dependent β-thalassemia (TDβ-T). Whole blood samples and clinical records were collected from 60 patients with TDβ-T and 20 healthy controls. Expression levels of selected LncRNAs were measured using qRT-PCR. Iron metabolism and erythropoiesis-related proteins were quantified using ELISA. TDβ-T patients exhibited significantly elevated levels of iron and erythropoiesis regulatory proteins, as well as increased expression of HAMP, GDF-15, FAM132B, and SLC40A1 compared to controls. Additionally, LncRNAs ANRIL, H19, LINCO133, MIAT, and NEAT1 were markedly upregulated, while LncRNA GAS5 was downregulated in patients with TDβ-T. Among these, LncRNAs NEAT1 and GAS5 showed the strongest diagnostic performance. A significant correlation was observed between the expression of HAMP and FAM132B and LncRNAs ANRIL, H19, LINCO133, and MIAT. Furthermore, LncRNA NEAT1 expression correlated positively with SLC40A1 and negatively with urea levels, whereas LncRNA GAS5 was inversely correlated with HAMP expression. This study is the first to demonstrate altered LncRNA expression patterns and their associations with iron metabolism, erythropoiesis regulatory proteins, and urea levels in patients with TDβ-T. These findings provide new insights for future research and potential therapeutic targets.
Liver fibrosis is a reversible wound-healing response to acute or chronic liver injury. Liver cirrhosis is the advanced stage of liver fibrosis. This study explored the causal associations of sex hormones - estradiol, bioavailable testosterone, total testosterone, and sex hormone-binding globulin (SHBG) - and adiponectin with liver fibrosis, cirrhosis, and primary biliary cirrhosis (PBC). A two-sample Mendelian randomization (MR) study using publicly available data was performed. Causal estimates were calculated by the inverse variance weighted (IVW) method, and additional approaches such as MR-Egger, weighted median, simple mode, and weighted mode were used to complement the IVW approach. Sensitivity analysis was performed employing leave-one-out analysis. The IVW analysis revealed a relationship between genetically predicted total testosterone levels and the likelihood of fibrosis and cirrhosis in females; odds ratio (OR) = 1.537, 95% confidence interval (CI): 1.082-2.182. There was a significant association between genetically predicted estradiol levels and an increased risk of liver fibrosis and cirrhosis (OR = 2.287, 95% CI: 1.403-3.727) and PBC (OR = 3.075, 95%CI: 1.306-7.240) in males. Our findings indicated that genetically predicted adiponectin was causally related to fibrosis and cirrhosis (OR = 1.608, 95% CI: 1.063-2.430) and PBC (OR = 2.631, 95% CI: 1.211-5.715). MR-Egger, weighted median, simple mode and weighted mode consistently yielded similar outcomes. Cochrane's Q test showed no heterogeneity in these instrumental variables, and there was no significant directional pleiotropy. There were positive causal associations of total testosterone with fibrosis and cirrhosis among females, and of estradiol levels with liver fibrosis and cirrhosis and PBC in males. Higher adiponectin could increase the risk of fibrosis and cirrhosis and PBC.
To evaluate global trends and SDI-related inequalities in the burden of ischemic heart disease (IHD) from 1990 to 2021, and project trajectories to 2035. This analysis provides crucial evidence to inform health policy and resource allocation for reducing future disparities. Using Global Burden of Disease (GBD) 2021 data, we analyzed IHD prevalence, incidence, deaths, and disability-adjusted life years (DALYs) across 204 countries. Analyses included temporal trends, decomposition, inequality assessment, and Bayesian projections. From 1990 to 2021, global age-standardized death rates declined annually by 1.3% and DALYs by 1.2%, while prevalence showed a slight increase (AAPC = 0.03%). High-SDI regions achieved the largest reductions, whereas low- and middle-SDI regions experienced persistent or rising burdens. Decomposition analysis indicated that population growth (110%) and aging (67%) were the main drivers of increasing DALYs, partially offset by epidemiological improvements (-77%). By 2035, despite continued declines in age-standardized rates, the absolute number of IHD cases is projected to increase by 18.2%. IHD remains a major global health challenge, with substantial SDI-driven disparities that persist despite overall progress. Strengthening prevention in low- and middle-SDI regions, addressing the growing healthcare demands of aging populations, and fostering sustained international collaboration are critical to reducing inequalities, guiding resource allocation, and ultimately alleviating the global burden.
Asthma and chronic obstructive pulmonary disease (COPD) are two common respiratory ailments with an overlapping pathogenesis. In this study, using a two-sample Mendelian randomization (MR) approach and analyzing publicly available genome-wide association study (GWAS) datasets, we explored the causal impact of asthma on the onset of COPD. Results: Using genetic instrumental variables associated with asthma (p < 5 × 10-8) and applying multiple MR methods (IVW, MR-Egger, and weighted median), we identified a significant causal relationship between asthma and COPD. The inverse variance weighted (IVW) method indicated that asthma increases the risk of developing COPD with an odds ratio (OR) of 1.35 (95% confidence interval [CI]: 1.12-1.58, p = 0.002). Additionally, multivariable MR analysis was performed to account for potential confounders, such as eosinophil count, smoking, and falls, which demonstrated that the association remains significant even after adjusting for these factors (OR = 1.29, 95% CI: 1.08-1.50, p = 0.004). This study provides robust evidence supporting the causal link between asthma and COPD, offering a more comprehensive understanding of their relationship.