Colorectal cancer is a common cause of cancer-related death worldwide. Thus, there is an urgent need to determine the mechanism of progression of colorectal cancer. In this study, we investigated the function and mechanism of long non-coding RNA LINC00958, providing a new biomarker for colorectal cancer. The expression of LINC00958, miR-3064-5p, and LEM domain containing 1 (LEMD1) in colorectal cancer tissues and cell lines was analyzed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). The interaction between LINC00958, miR-3064-5p, and LEMD1 was assessed using the luciferase assay. The viability, proliferation, migration, invasion, and apoptosis of colorectal cancer cells with silenced LINC00958, miR-3064-5p, and LEMD1 were investigated using the cell counting kit-8 (CCK-8), 5′-Bromo-2′-deoxyuridine (BrdU), flow cytometry, wound healing, and transwell assays. Phosphorylated phosphoinositide 3-kinase (p-PI3K) and phosphorylated protein kinase B (p-AKT) protein levels were measured by western blotting. LINC00958 and LEMD1 were found to have increased, while the expression of miR-3064-5p was decreased in colorectal cancer tissues and cell lines. Silencing of LINC00958 hampered cell viability, proliferation, migration, and invasion, while enhancing the apoptosis in colorectal cancer cells. Notably, LINC00958 inhibited miR-3064-5p and promoted LEMD1; the miR-3064-5p inhibitor abrogated the effect of LINC00958 silencing in colorectal cancer cells. Additionally, LEMD1 knockdown inhibited the activation of PI3K/AKT signaling. Our analyses have shown that LINC00958 could facilitate the progression of colorectal cancer by sponging miR-3064-5p and releasing LEMD1, leading to the activation of the PI3K/AKT pathway. Thus, LINC00958 may be considered as an effective biomarker for the treatment of colorectal cancer.

Background. Gastric cancer pathological biopsy and visual examination have been the gold standard for gastric cancer diagnosis, but their operation is costly, demanding, and risky, so it is especially important to find an effective examination method in clinical practice. Aims. To investigate the correlation between serum pepsinogen I (PGI), pepsinogen II (PGII), pepsinogen I and II ratio (PGR), IL-6, and TNF-α and Helicobacter pylori (Hp) infection in patients with gastric cancer. Materials and Methods. Fifty patients with Hp-infected gastric cancer admitted to the Department of Gastroenterology of our hospital from January 2019 to December 2021 were selected for the study as the observation group, and another 50 patients without Hp-infected gastric cancer were selected as the comparison group to compare the correlation analysis of PGI, PGII, PGR, IL-6, and TNF-α with Hp infection between the two groups after admission and treatment. Results. After measurement, PGI and PGII in the observation group were significantly lower than those in the comparison group, and TNF-α, IL-18, and IL-6 in the observation group were significantly higher than those in the comparison group, and the comparative differences were all statistically significant ( P < 0.05 ). The results of multivariate logistic regression model analysis of independent risk factors for gastric cancer showed that IL-18, hs-CRP, and tumor necrosis factor- (TNF-) α were risk factors for Hp infection in gastric cancer. Conclusion. The expression of IL-18, hs-CRP, and TNF-α factors in Hp-infected gastric cancer patients is correlated. IL-6, IL-18, and TNF-α are involved in the entire process from the onset to the development of Hp-positive gastric mucosal inflammation in patients, which is of great value in the diagnosis of gastric cancer and helps to assess the degree of progression and prognosis of gastric cancer.

Circular RNAs (circRNAs) frequently participate in pancreatic cancer (PC) progression. This study focuses on circ_0000106, a novel circRNA, and its potential function in PC development. Circ_00001106, miR-455–3p, and HDAC4 expression levels in PC were determined using qRT-PCR and immunoblotting. RNA immunoprecipitation and dual-luciferase reporter assays were performed to verify their binding interactions. Loss-of-function assays, including CCK-8, colony formation, and transwell assays, were used to estimate the proliferative and migratory properties of PC cells. A nude mouse model was constructed to assess the influence of circ_0000106 on tumor formation in vivo. A pronounced elevation of circ_0000106 and HDAC4 and a reduction of miR-455–3p in PC were observed. Circ_0000106 was prone to binding to miR-455–3p, and miR-455–3p further targeted HDAC4. Functionally, the proliferative and migratory properties of PC cells were dampened by the loss of circ_0000106 or HDAC4 and could be potentiated by miR-455–3p inhibition. Moreover, the knockdown of circ_0000106 delayed tumor growth in vivo. Additionally, the downregulation of miR-455–3p attenuated the repressive effects of circ_0000106 deficiency on PC cell migration and proliferation. Loss of HDAC4 exerted similar mitigative effects on miR-455–3p downregulation-stimulated PC cells. In conclusion, circ_0000106 promotes tumor migration and growth in PC by targeting the miR-455–3p/HDAC4 axis. These results suggest that the circ_0000106/miR-455–3p/HDAC4 network could be regarded as a latent target for PC treatment.

Objective: To investigate the significance of serum bilirubin in the diagnosis of atypical acute appendicitis. Methods: perform a retrospective analysis of 120 patients with atypical acute appendicitis diagnosed in our hospital from July 2012 to July 2016. All patients underwent routine liver function tests before surgery. Results: 83 patients were confirmed by surgery as acute appendicitis, of which 68 patients had elevated serum total bilirubin and direct bilirubin, and 15 patients were normal; 37 patients were confirmed by surgery as non-acute appendicitis, of which 7 patients had elevated serum total bilirubin and direct bilirubin, and 30 patients were normal. Conclusion: The increase of serum bilirubin level has certain clinical significance for the diagnosis of atypical acute appendicitis.

Objective: To summarize the experience without hemorrhage after PPH of 218 patients with mixed hemorrhoid. Methods: PPH (Procedure for prolapse and hemorrhoids) was performed routinely. During operation, it is paid attention that the hemorrhoid artery should be completely mutilated, the anastomat should be squeezed before and after the anastomosis, the anastomosis should be carefully examined, the hemostasis should be completely performed, and relevant hemostasis measures should be taken after the operation. Results: None of the 218 patients had postoperative hemorrhage. Conclusion: Relevant measures can be taken after operation to prevent the occurrence of postoperative hemorrhage.