Background: Dysphagia is a common functional impairment in elderly populations, often leading to severe complications such as malnutrition and aspiration pneumonia, significantly increasing healthcare burdens. Currently, effective prognostic assessment tools are lacking. The absolute lymphocyte count (ALC), a biomarker reflecting immune-nutritional status, has potential predictive value in this context, though its role in dysphagia prognosis remains unclear. Methods: This retrospective cohort study included 253 dysphagic patients who received percutaneous endoscopic gastrostomy (PEG) or total parenteral nutrition (TPN) between 2014 and 2017. Five patients with missing ALC were excluded. Cox regression models assessed the association between ALC and mortality. ALC was analyzed as both continuous variable (using restriocted cubic splines) and categorical tertiles, with additional threshold analyses to assess non-linearity. Kaplan–Meier survival curves and subgroup analyses were also performed. Results: Lower ALC was associated with poorer nutritional status, higher inflammatory markers, and greater comorbidity burden. Higher ALC was independently associated with reduced mortality (adjusted HR: 0.60; 95% CI: 0.44–0.83; p = 0.002). Patients in the highest tertile had significantly better survival than those in the lowest (HR: 0.37; 95% CI: 0.23–0.59; P < 0.001). A non-linear threshold effect was identified at ALC = 1.899×10⁹/L (p for non-linearity = 0.009). Kaplan–Meier analysis confirmed improved survival with higher ALC (p < 0.0001). Subgroup analyses showed the protective effect of higher ALC was consistent across age, sex, BMI, PEG use, and comorbidity strata, with no significant interactions. Conclusions: ALC is an independent, non-linear predictor of mortality in older dysphagic patients and may aid clinical risk stratification across diverse patient subgroups.

Background: Hepatocellular carcinoma (HCC) faces significant challenges in early diagnosis and prognostic assessment, necessitating novel molecular biomarkers. The role of GCN1 in tumorigenesis remains unclear, warranting systematic investigation of its clinical value. Methods: Utilizing multi-omics data from 164 HCC patients in the TCGA database, we comprehensively evaluated the diagnostic and prognostic value of GCN1 through differential expression analysis, Cox proportional hazards regression, and gene set enrichment analysis (GSEA). Results: GCN1 expression was significantly upregulated in tumor tissues (P<0.001), with ROC analysis demonstrating an AUC of 0.921 (95% CI: 0.893-0.950) for discriminating tumor from normal tissue. Clinical correlation analysis revealed that high GCN1 expression significantly associated with advanced T stage (OR=1.941, P=0.002) and AFP levels >400 ng/ml (OR=3.697, P<0.001). Multivariate survival analysis confirmed its independent prognostic value (HR=1.454, P=0.038). Functional analysis indicated GCN1 promotes tumor progression by regulating cell cycle (NES=2.385) and axon guidance (NES=2.307) pathways. Conclusion: This study first elucidates the dual clinical value of GCN1 in HCC, providing a theoretical foundation for developing novel diagnostic biomarkers and prognostic evaluation systems. Future research should validate its molecular mechanisms and explore potential targeted therapies.