Background and aims: The effectiveness of emergent endoscopy (EE), defined as endoscopy performed within six hours of admission, for improving outcomes in patients presenting with acute upper gastrointestinal bleeding (AUGIB) remains controversial. This study aimed to evaluate the impact of EE on 42-day rebleeding and mortality rates and identify subgroups of patients who benefit most from this approach.
Methods: We conducted a retrospective cohort study at a tertiary hospital with 24/7 endoscopy services. Eligible patients were aged ≥18 years, presented with AUGIB, and underwent endoscopy within 24 hours of admission. The exclusion criteria included prior interventions at other facilities, in-hospital bleeding for unrelated reasons, or loss to follow-up. All patients were managed under a standardized AUGIB protocol. The primary outcomes were 42-day rebleeding and mortality. The data were analysed via multivariate logistic regression and interaction analyses.
Results: There were 651 patients with a median age of 58.6 years (18-92). The median time from admission to endoscopy was 4.8 hours (3.1-8.0). The 42-day rebleeding and mortality rates were 16.7% and 11.8%, respectively. EE was significantly associated with 42-day mortality but not rebleeding. Independent risk factors for mortality included hemodynamic instability, malignancy, NSAID use, and elevated serum creatinine. Interaction analysis revealed that EE was associated with reduced 42-day mortality in hemodynamically unstable patients (OR: 0.29, 95% CI: 0.145-0.579), a benefit not observed in patients with other risk factors for mortality.
Conclusion: EE appears to be associated with reduced 42-day mortality in patients presenting with hemodynamically unstable AUGIB.
Objective: This study aimed to investigate the expression of BEND3 in hepatocellular carcinoma (HCC), its correlation with clinical characteristics, and its functional and mechanistic impacts on HCC progression.
Methods: Bioinformatics analyses identified BEND3 as highly expressed in HCC and associated with poor clinical prognosis, which was further validated using qRT-PCR, western blotting and immunohistochemistry. Stable BEND3-overexpressing and silenced cell lines were constructed to evaluate its functional effects. CCK-8 and colony formation assays assessed its influence on cell proliferation, while wound healing and Transwell assays evaluated its role in migration and invasion. WB and immunofluorescence were employed to analyze the effects of BEND3 on epithelial-mesenchymal transition (EMT) and the PI3K/AKT/mTOR signaling pathway.
Results: Public database analysis, alongside qRT-PCR, western blotting, and immunohistochemical, confirmed that BEND3 expression is significantly elevated in HCC tissues compared to normal liver tissues and is closely associated with poor prognosis. Functional assays demonstrated that BEND3 promotes HCC cell proliferation, migration, and invasion. Mechanistic studies revealed that BEND3 drives HCC progression by inducing EMT and activating the PI3K/AKT/mTOR signaling pathway.
Conclusion: BEND3 is highly expressed in HCC and strongly correlates with poor clinical outcomes. Functional and mechanistic analyses indicate that BEND3 enhances HCC progression by promoting proliferation, migration and invasion via EMT induction and PI3K/AKT/mTOR pathway activation.