Hepatocellular carcinomas(HCC) consisted of heterogeneous subtypes with different recurrence probabilities after liver transplantation(LT). Our study aimed to develop an improved model for predicting the recurrence of solitary HCC after LT. In this retrospective study, 151 solitary HCC patients who received orthotopic LT over a period of 10 consecutive years were included. All recipients received graft from deceased donors. The first eligible 50 patients were used as validation cohort and others were utilized to construct the model. A two-tailed P < 0.05 was considered to indicate statistical significance for all analysis. Based on the maximisation of the Youden’s index, the optimal cutoff values for alpha-fetoprotein(AFP) and tumor diameter were 261.6 ng/mL and 3.6 cm, respectively. Vascular involvement includes gross and microscopic vascular invasion. Variables potentially affecting recurrence-free survival(RFS) were examined using univariate and multivariate Cox regression analysis. Univariate and multivariate analysis revealed that AFP, tumor diameter, vascular invasion and cytokeratin-19/glypican-3 sub-typing were independent prognostic factors for RFS, thus comprised the risk scoring model. The AUC values of the model in the cohorts were significantly higher than that of the Milan, UCSF, Fudan and Hangzhou criteria. These findings suggest the model has high performance in predicting early recurrence of solitary HCC patients after LT.

Emerging evidence links gut microbiota (GM) to venous thromboembolism (VTE), deep vein thrombosis (DVT), and pulmonary embolism (PE), but causal insights are limited. Using two-sample Mendelian randomization (MR), we assessed causal effects of 211 GM taxa and 489 plasma metabolites on VTE/DVT/PE. Genetic instruments (single nucleotide polymorphism) for GM and metabolites were leveraged to infer causality, complemented by mediation and pathway analyses. Sixteen GM taxa (e.g., protective Firmicutes, Clostridia; risk-enhancing Bacteroidetes, Desulfovibrionaceae) and 40 metabolites showed causal associations with VTE/DVT/PE. Reverse MR identified 11 GM changes secondary to thrombosis. No pleiotropy or heterogeneity was detected. Ten metabolite-mediated pathways (e.g., arginine biosynthesis) bridged GM to thrombosis, suggesting GM-metabolite interactions as potential biomarkers for thrombotic risk stratification and prognosis.

The rising incidence of liver cirrhosis among women of childbearing age is associated with increased maternal morbidity and potential adverse maternal health outcomes. This study aimed to analyze temporal trends of cirrhosis incidence and project future epidemiological patterns to guide targeted prevention and control strategies. We extracted liver cirrhosis incidence data from the Global Burden of Disease Study 2021, covering 204 countries and territories from 1992 to 2021. The analytical population included females aged 15 to 49 years. Trends across age groups, periods, and birth cohorts were analyzed using the age-period-cohort model. The Bayesian age-period-cohort model was utilized to forecast epidemiological trends through 2030. Between 1992 and 2021, global cirrhosis trends varied by etiology: alcohol-related cases increased (14,566.88–19,340.29) despite declining age-standardized incidence rates (1.22–0.94 per 100,000), while nonalcoholic fatty liver disease-related cirrhosis showed a continuous upward trend in both case counts and age-standardized incidence rate between 1992 and 2021 (reaching 16,095,135.50 cases and 831.02 per 100,000 population in 2021), with projections indicating it may rise to approximately 19.63 million cases (95% uncertainty interval = 16.36 million–22.89 million) by 2030. Low socio-demographic index regions bore the highest burden. Projections through 2030 suggest a potential rising global burden, particularly for alcohol-related cases, with divergent trends projected for China (decreasing) and India (increasing). The global incidence of liver cirrhosis among women of childbearing age is rising, in population-level correlation with the growing burden of nonalcoholic fatty liver disease and regional gaps in viral and alcohol-related cirrhosis etiologies. These findings highlight the potential need for region-specific prevention strategies. Limitations include Global Burden of Disease data quality, ecological bias, and insufficient pregnancy-specific data for detailed incidence trend analysis.