Role of immune related genes in predicting prognosis and immune response in patients with hepatocellular carcinoma.

Immunotherapy has developed rapidly in recent years. This study aimed to establish a prognostic signature for immune-related genes (IRGs) and explore related potential immunotherapies. The RNA-seq transcriptome profiles and clinicopathological information of patients were obtained from The Cancer Genome Atlas. Differentially expressed IRGs in tumors and normal tissues were screened and a risk score signature was constructed to predict the prognosis in patients with hepatocellular carcinoma (HCC). Receiver operating characteristic curves, survival analyses, and correlation analyses were used to explore the clinical application of this model. We further analyzed the differences in clinical characteristics, immune infiltration, somatic mutations, and treatment sensitivity between the high- and low-risk populations characterized by the prognostic models. The immune cell infiltration score and immune-related pathway activity were calculated using the single sample gene set enrichment analysis (ssGSEA) set enrichment analysis. Gene ontology (GO), Kyoto encyclopedia of genes and genomes, and GSEA were used to explore the underlying mechanisms. We constructed a nine-IRG formula to predict the prognosis in HCC patients. The higher the risk score, the higher the malignancy of the tumor and the worse the prognosis. There were significant differences in immune related processes between the high- and low-risk groups. TP53 and CTNNB1 mutations were significantly different between different risk groups. The expression of model gene was closely related to the sensitivity of tumor cells to chemotherapeutic drugs. This risk score model, which is helpful for the individualized treatment of patients with different risk factors, could be a reliable prognostic tool for HCC patients.

Helicobacter pylori infection increases the risk of nonalcoholic fatty liver disease in diabetic population.

Background: The effect of Helicobacter pylori (H. pylori) on nonalcoholic fatty liver disease (NAFLD) in the population is still controversial. Diabetes and NAFLD are both metabolically related diseases, and no studies have classified the population to study the effect of H. pylori infection on NAFLD in diabetics. Methods: A population of people who were examined in the Taizhou Hospital Health Examination Center from 2017 to 2022 was included, and hematological indicators, body parameters, ultrasound data, and H. pylori detection by urea nitrogen test were collected from patients. All physical examination populations were divided into diabetic and non-diabetic populations. Results: After multivariate logistic regression, H. pylori infection remained an independent risk factor for NAFLD in diabetics, but it had no significant effect on NAFLD in non-diabetic population. Additionally, there was a nonlinear relationship between glycosylated hemoglobin and H. pylori infection in diabetic population. Moreover, the incidence of NAFLD in diabetics increased with persistent H. pylori infection. Conclusion: In the diabetic population, H. pylori infection does increase the risk of developing NAFLD. Glycemic control and eradication of H. pylori infection may have positive implications for reducing the incidence of NAFLD in diabetic population.

Effect of baicalin on proliferation and apoptosis in pancreatic cancer cells.

BACKGROUND AND OBJECTIVES: Pancreatic cancer is one of the most lethal cancer types. Pancreatic cancer is highly malignant and characterized by rapid and uncontrolled growth. This study was designed to investigate the effect of baicalin on proliferation and apoptosis in pancreatic cancer cells. METHODS: CCK-8 assay and Clone formation assay were performed to detect the effect of baicalin on proliferation in pancreatic cancer cells. Cell invasion and migration were all assessed with Wound healing assay and Transwell invasion assay. Flow Cytometry Analysis and DAPI staining were performed to detect the effect of baicalin on apoptosis in pancreatic cancer cells. Furthermore, proliferation-associated protein and apoptosis-related protein were detected to evaluate the cell proliferation and apoptosis levels. P-JNK protein, t-JNK protein, Foxo1 protein and BIM protein were examined by western blot to verify whether baicalin could regulate the proliferation and apoptosis via the JNK/Foxo1/BIM signaling pathway in pancreatic cancer cells. RESULTS: The cell proliferation level was significantly decreased while the cell apoptosis level was significantly increased in pancreatic cancer SW1990 cells treated with baicalin. As the same, baicalin downregulated the ability of invasion and migration in pancreatic cancer SW1990 cells. CONCLUSION: Baicalin might inhibit cell proliferation and promote cell apoptosis via JNK/Foxo1/BIM signaling pathway in pancreatic cancer SW1990 cells.