Early gastric cancer is associated with a much better prognosis than advanced disease, and strategies to improve prognosis is strictly dependent on earlier detection and accurate diagnosis. Therefore, a label-free, non-invasive imaging technique that allows the precise identification of morphologic changes in early gastric cancer would be of considerable clinical interest. In this study, multiphoton microscopy (MPM) using two-photon excited fluorescence combined with second-harmonic generation was used for the identification of early gastric cancer. This microscope was able to directly reveal improved cellular detail and stromal changes during the development of early gastric cancer. Furthermore, two features were quantified from MPM images to assess the cell change in size and stromal collagen change as gastric lesion developed from normal to early cancer. These results clearly show that multiphoton microscopy can be used to examine early gastric cancer at the cellular level without the need for exogenous contrast agents. This study would be helpful for early diagnosis and treatment of gastric cancer, and may provide the groundwork for further exploration into the application of multiphoton microscopy in clinical practice.

In the present study, imatinib mesylate (IM) was used to induce resistance in the gastrointestinal stromal tumour (GIST) cell line, GIST‑T1, to establish a stable resistant cell line. The growth characteristics and expression profile of the established cell line were compared with those of the parental cell line. Additionally, the resistance mechanism of the gastrointestinal stromal tumours was preliminarily investigated. The GIST‑T1 cells were cultured in vitro, and the drug was administered in the logarithmic phase of cell growth using intermittent dosing with increasing concentrations to obtain a drug‑resistant cell line by repeated induction. Differences in the biological behaviours of the parental cells and drug‑resistant cells were examined, and changes in the expression profiles were compared in the two cell lines. The results showed that the IM‑resistant GIST‑T1 cell line (GIST‑T1 IR) was successfully established. Analysis of the biological behaviours of the two cell lines revealed that the average doubling times of the parental cells and drug‑resistant cells were 26.59 and 33.63 h, respectively. The results of a scratch migration assay revealed that the migration ability was enhanced in the GIST‑T1 IR cells. The results of CCK‑8 detection indicated that the half maximal inhibitory concentration values of the two types of cells were 10.5 and 42.0 µM, respectively, which represented an increase of ~4‑fold in the GIST‑T1 IR cells. Flow cytometric cell cycle analysis indicated that the numbers of cells in the G0/G1, S and G2 phases increased following the induction treatment. Taken together, an IM-resistant GIST T1 cell line was successfully established, which opens novel avenues for individualized tumour chemotherapy.

Glycemic control plays a crucial role in the outcomes of acute pancreatitis (AP), yet traditional glucose metrics have shown limited prognostic value. This study investigates the association between mean glucose area under the curve (AUC) and mortality outcomes in AP patients. We conducted a retrospective cohort study of 1085 intensive care unit patients with AP using data from the Medical Information Mart for Intensive Care IV database. Patients were stratified into tertiles based on mean glucose AUC. Multivariable Cox regression and restricted cubic spline analyses were employed to assess the relationship between mean glucose AUC and mortality outcomes. Predictive performance was quantified using receiver operating characteristic curve analysis, and robustness was further tested through comprehensive subgroup and sensitivity analyses. A higher mean glucose AUC was significantly associated with increased mortality risk. In the fully adjusted model, the hazard ratio for in-hospital mortality was 1.10 (95% confidence interval: 1.08–1.12; P < .001). Compared with the lowest tertile, patients in the highest tertile demonstrated an 11.12-fold increased mortality risk (95% confidence interval: 5.78–21.41; P < .001). Mean glucose AUC showed superior discriminative capacity for predicting in-hospital mortality (AUC = 0.783) compared with other glucose metrics. The association remained robust across various subgroups and sensitivity analyses. Mean glucose AUC serves as a powerful, independent predictor of in-hospital mortality in AP patients. This novel metric outperforms conventional glucose parameters in prognostic accuracy, suggesting its potential utility in clinical risk stratification and treatment optimization.

Objectives: Cirrhosis signifies a critical phase in liver disease with high mortality, particularly in patients admitted to intensive care unit (ICU). Red cell distribution width (RDW) demonstrates prognostic value in various conditions, with evidence linking it to inflammation and adverse outcomes in liver disease. However, the predictive utility of RDW and its derived indices in patients with cirrhosis admitted to ICU remains undetermined. This study investigated the associations between RDW-related biomarkers and prognosis in critically ill cirrhosis patients. Methods: A retrospective analysis used data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, including 1,871 adults with cirrhosis at first ICU admission. The analyzed biomarkers were RDW, RDW-to-albumin ratio (RAR), RDW-to-platelet ratio (RPR), and hemoglobin-to-RDW ratio (HRR). The primary outcome was 30-day all-cause mortality; secondary outcomes were 90-day, and 365-day mortality. Adjusted multivariate Cox regression models determined biomarker-mortality associations. Receiver operating characteristic (ROC) curve analyses evaluated predictive performance of the biomarkers. Results: The cohort had a mean age of 58.8 ± 12.3 years and 64.8% of the patients were male. The mortality rates were 31.8% (30-day), 39.3% (90-day), and 48.0% (365-day). Mortality was consistently higher in high versus low RDW groups. After multivariable adjustment, all biomarkers were independently associated with 30-day, 90-day, and 365-day mortality, respectively. When expressed per SD, RDW (HR 1.41, 95% CI 1.30–1.52), RAR (HR 1.17, 95% CI 1.11–1.24), RPR (HR 1.19, 95% CI 1.11–1.28), and HRR (HR 0.52, 95% CI 0.44–0.61) were each significantly associated with 30-day mortality. ROC analysis revealed RDW had the highest predictive value (AUC 63.3%), followed by HRR (AUC 61.7%), RAR (AUC 59.6%), and RPR (AUC 55.6%). RDW demonstrated the highest discriminative ability for 30-day mortality, with incremental predictive value when combined with established scores (absolute AUC increase 0.68–1.58%). Conclusion: RDW-related biomarkers demonstrate statistically significant but modest associations with mortality in ICU cirrhosis patients. RDW and HRR showed the strongest predictive capabilities among the four indices, though standalone discrimination was limited. These accessible, cost-effective biomarkers may serve as adjunctive prognostic markers when combined with established scoring systems. However, further prospective validation is required before clinical implementation, and dynamic changes in these biomarkers warrant investigation in future studies.

Background: The triglyceride-glucose (TyG) index, a simple and validated surrogate marker of insulin resistance, may be clinically relevant to colorectal polyp development because insulin resistance can promote colorectal neoplasia through hyperinsulinemia, chronic inflammation, oxidative stress, and dysregulated insulin-like growth factor signaling. However, the relationship between TyG index and colorectal polyps remains incompletely understood. This study aimed to investigate the association between TyG index and colorectal polyp risk using both observational and genetic approaches. Methods: We conducted a cross-sectional study of 4,263 patients undergoing colonoscopy. Associations between TyG index and colorectal adenomatous polyps were assessed using multivariable logistic regression. A two-sample Mendelian randomization (MR) analysis evaluated potential causal effects, with inverse-variance weighted (IVW) method as primary analysis and multiple sensitivity analyses. Results: Although the crude distribution of colorectal polyps across TyG quartiles did not show a strictly monotonic pattern, participants in different TyG quartiles differed substantially in age, sex distribution, BMI, lifestyle factors, comorbidities, and metabolic profiles. Therefore, multivariable logistic regression was performed to account for potential confounding. Higher TyG index was significantly associated with increased prevalence of colorectal adenomatous polyps after full adjustment (odds ratio [OR] 1.13, 95% CI: 1.01–1.27; P-trend = 0.032). Restricted cubic spline analysis showed no evidence of a nonlinear association between the TyG index and colorectal adenomatous polyp risk (P for nonlinearity = 0.459), supporting the use of a linear model in this dataset. MR analysis supported a observational and potential causal association between genetically predicted TyG index and colon polyps (inverse-variance weighted OR: 1.20, 95% CI: 1.10–1.31; P < 0.001), with consistent results across sensitivity analyses and no evidence of directional pleiotropy (P = 0.884). However, no significant association was found for rectal polyps. Conclusion: Both observational evidence and genetic evidence support a positive association between the TyG index and colon polyps, whereas the MR analysis did not provide evidence for a causal association with rectal polyps. These findings suggest the potential utility of the TyG index in risk stratification and underscore the role of insulin resistance in the pathogenesis of colorectal neoplasia.