First Affiliated Hospital of Guangxi Medical University

Anastomotic leakage (AL) is a devastating complication of gastrointestinal surgery and a critical source of hospital-acquired infections. This review synthesizes recent advances in AL management, with a focus on infection-targeted strategies. A narrative review of the literature was conducted, encompassing established clinical therapies and emerging preclinical innovations. For mature endoscopic modalities, such as Endoscopic Vacuum Therapy (EVT), clinical cohort data and meta-analyses support high fistula closure rates (74-94.4%) and a significant reduction in sepsis risk. In parallel, novel preclinical strategies-including antibiotic-eluting hydrogels, reversible endoscopic bypass procedures, and artificial intelligence-driven prediction models-demonstrate transformative potential in early-stage studies but require robust clinical validation. The future management of AL is evolving towards an integrated model, combining evidence-based endoscopic interventions with intelligent biomaterial-based approaches. Translating preclinical innovations into practice will necessitate overcoming challenges related to cost, standardization, and long-term safety, ultimately enabling a paradigm shift from reactive repair to proactive, precision prevention.

To explore the clinical significance of new haematological indicators, including rheumatoid arthritis-specific citrullinated protein (RA-CP), haemoglobin-to-red cell distribution width ratio (HRR), and mean platelet volume/platelet count (MPV/PC) ratio, in rheumatoid arthritis (RA). This study is the first to evaluate the combined diagnostic utility of RA-CP and HRR in RA.

Data from 700 subjects, including RA patients, patients with other autoimmune diseases, and healthy controls, were retrospectively analyzed. The relationships between these indicators and the risk of RA were assessed using logistic regression, correlation, and receiver operating characteristic (ROC) curve analyses.

There were significant differences in RA-CP, HRR, and MPV/PC among the three groups (p < 0.001, for all). Logistic regression analysis indicated RA-CP and HRR as independent predictors of RA (p < 0.001, for both). Moreover, RA-CP and HRR were closely associated with the clinical characteristics. In addition, ROC curve analysis revealed that the combined detection of RA-CP, HRR, and anti CCP antibody achieved the highest area under the ROC curve (AUC_{RA - CP + HRR + antiCCP antibody} = 0.998) for the diagnosis of RA and also improved the diagnostic sensitivity (98.31%).

RA-CP and HRR were identified as independent predictors of RA, including RA-CP as a risk factor for RA and HRR as a protective factor for RA. Combined detection of RA-CP, HRR, and anti-CCP antibody could enhance the accuracy and sensitivity of laboratory diagnosis. Although MPV/PC did not demonstrate significant independent predictive value in this study, this represents the first exploration of its potential clinical role in RA.

Glycine C-acetyltransferase (GCSH), a component of the mitochondrial glycine cleavage system, has been previously linked to cuproptosis or tumor progression, but its role in colorectal cancer (CRC) remains incompletely understood. We analyzed GCSH expression across multiple CRC datasets, including the TCGA dataset (n = 689) and four independent GEO datasets (total n = 709), and validated findings in clinical tissues, blood samples, and CRC cell lines. Functional roles of GCSH were assessed using CCK-8, wound healing, and Transwell assays. Cuproptosis was induce, and evaluated by flow cytometry, Western blotting, and measurement of intracellular Cu²⁺, ROS, and FDX1 levels. The regulatory relationship between GCSH and FDX1, as well as the involvement of the PI3K/AKT pathway, was explored through rescue experiments and molecular docking analysis. The analysis of Bulk RNA-seq data and scRNA-seq datasets revealed the expression and the biological function of GCSH in CRC. The validation experiments confirmed that GCSH was consistently overexpressed in CRC tissues and blood samples, and its expression correlated with distant metastasis. GCSH knockdown inhibited cell viability, migration, and invasion, with minimal effects on apoptosis. Mechanistically, GCSH suppressed cuproptosis by downregulating FDX1 protein and reducing intracellular Cu²⁺ and ROS accumulation. Molecular docking suggested a potential interaction between GCSH and FDX1. Furthermore, GCSH was identified as a downstream effector of PI3K/AKT pathway, mediating its protective effect against cuproptosis. GCSH promotes CRC progression and confers resistance to cuproptosis via the PI3K/AKT-GCSH/FDX1 axis. These findings identify GCSH as a novel regulator of cuproptosis and a potential therapeutic target in CRC.