Esophagogastric variceal bleeding (EGVB) is one of the main complications of portal hypertension, especially in patients with liver cirrhosis, and has a very high fatality rate. At present, the treatment methods for rupture and bleeding of gastroesophageal varices (GV) include drug therapy, compression hemostasis with three-lumen and two-balloon tube, endoscopic therapy, and interventional and surgical operations. Endoscopy and intervention or their combined application is the mainstream treatment modes in clinical practice, especially their combined application has been increasingly recognized by front-line clinicians. This article intends to discuss the application characteristics of the two treatment methods.
Background. Colorectal cancer is highly prevalent and causes high global mortality, and glucagon axis has been implicated in colon cancer. The present study is aimed at investigating the regulating mechanisms of glucagon involvement in colorectal cancer. Methods. Publicly available data from the TCGA database was utilized to explore the expression pattern and regulating role of glucagon (GCG) in colorectal cancer (COADREAD) including colon adenocarcinomas (COAD) and rectum adenocarcinomas (READ). Statistical analyses were performed using the R software packages and public web servers. The expression pattern and prognostic significance of GCG gene in pan-cancer and TCGA-COADREAD data were investigated by performing unpaired and paired sample analyses. The association of GCG expression with clinical characteristics was investigated using logistic regression analysis. Univariate cox regression analysis was performed to test the prognostic value of GCG expression for overall survival in COADREAD patients. GCG-significantly correlated genes were obtained. Biological functions and signaling pathways were identified by performing functional enrichment analysis and Gene Set Enrichment Analysis (GSEA). Additionally, the potential involvement of GCG in tumor immunity was researched by investigating the correlation between GCG expression and 24 tumor infiltrating immune cells. Results. GCG was found to be significantly downregulated in COADREAD tumor samples compared with healthy control samples. GCG gene was shown to be associated with the prognostic outcomes of COADREAD, whereby its upregulation predicted improved survival outcomes. Functional enrichment analysis showed that the top 100 positively and top 100 negatively GCG-correlated genes were mainly enriched in three signaling pathways including ribosome, nitrogen metabolism, and proximal tubule bicarbonate reclamation. The GSEA showed that GCG-significantly correlated genes were mainly enriched in cell cycle-related pathways (reactome cell cycle, reactome cell cycle mitotic, reactome cell cycle checkpoints, reactome M phase, Reactome G2 M DNA damage checkpoint, and Reactome G2 M checkpoints), neuropeptide ligand receptor interaction, RHO GTPases signaling, WNT signaling, RUNX1 signaling, NOTCH signaling, ESR signaling, HCMV infection, and oxidative stress-related signaling. GCG was positively correlated with Th17 cells, pDC, macrophages, TFH cells, iDC, Tem, B cells, dendritic cells, neutrophils, mast cells, and eosinophils and was negatively associated with NK cells. Conclusions. GCG dysregulation with high prognostic value in COADREAD was noted. Several tumor progression-related pathways and tumor immune-modulatory cells were linked to GCG expression in COADREAD. Therefore, GCG may be regarded as a potential therapeutic target for treating colorectal cancer.
Objective. To investigate the relationship between angiotensin II (Ang II), vascular endothelial growth factor (VEGF), and arteriosclerosis obliterans (ASO). Methods. 60 ASO patients diagnosed and treated from October 2019 to December 2021 were selected for the observation group while 30 healthy physical examiners were for the control group. The general information (gender, age, history of smoking, diabetes, and hypertension) and arterial blood pressure (systolic and diastolic blood pressure) of the two groups were collected, and parameters like disease site and duration, Fontaine stage, and ankle-brachial index (ABI) of ASO patients have been evaluated. Ang II, VEGF, uric acid (UA), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), and total cholesterol (TC) were also detected for the two groups. The variations in UA, LDL, HDL, TG, and TC among two groups along with levels of Ang II and VEGF in ASO patients in accordance to conditions like the general situation, disease duration, disease site, Fontaine stage, and ABI risk level have been studied to establish a correlation between Ang II and VEGF and ASO. Results. (1) The proportion of males with a history of smoking, diabetes, and hypertension was higher ( P < 0.05 ) among ASO patients in comparison to the control group. The diastolic blood pressure, LDL, TC, Ang II, and VEGF levels were found to be higher ( P < 0.05 ) whereas HDL was low ( P < 0.01 ). (2) The level of Ang II in male patients with ASO was significantly higher than that in female ASO patients ( P < 0.05 ). In ASO patients, the levels of Ang II and VEGF increased not only with age ( P < 0.01 ) but also with progression in Fontaine stages II, III, and IV ( P < 0.01 ). (3) Logistic regression analysis revealed Ang II and VEGF as risk factors for ASO. (4) An AUC (area under the ROC (receiver operator characteristic) curve) for Ang II and VEGF for the diagnosis of ASO was 0.764 (good) and 0.854 (very good), respectively, while their combined AUC in diagnosing ASO was 0.901 (excellent). The AUC of Ang II and VEGF together in diagnosing ASO was greater than that of Ang II and VEGF alone along with higher specificity as well (all P < 0.05 ). Conclusion. Ang II and VEGF were correlated with the occurrence and development of ASO. The AUC analysis demonstrates that Ang II and VEGF were highly discriminative of ASO.
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