Analysis of gastroscopy results among healthy people undergoing a medical checkup: a retrospective study.

BACKGROUND: The association of upper gastrointestinal endoscopic findings with sex, age, and Helicobacter pylori infection in asymptomatic healthy people is unclear. The aim of this study was to retrospectively determine the associations of upper gastrointestinal endoscopic findings in asymptomatic healthy people with sex, age, and H. pylori infection. METHODS: A retrospective study was conducted on 2923 patients from a health examination center in Xiangya Hospital between September 2015 and September 2019. Data on sex, age, H. pylori infection, and gastroscopy results were collected. RESULTS: Among 2923 asymptomatic patients who underwent gastroscopy, 2911 (99.59%) had abnormal results. The top three results were chronic gastritis (95.11%), peptic ulcer (17.45%), and duodenitis (9.17%). Inflammation of the gastric mucosa in chronic gastritis was more severe in the H. pylori-positive group. The incidence of peptic ulcer decreased with increasing age and was higher in men, patients aged < 30 years, and H. pylori-positive patients. The incidence of polyps was higher in women (9.54%) than in men (5.94%), and the incidence in individuals aged ≥60 years (11.63%) was higher than that in those aged < 60 years (6.83%). The pathological results of gastric polyps depended on the location of the lesion. CONCLUSION: The incidence of abnormal upper gastrointestinal endoscopic results is high in asymptomatic healthy people undergoing a check-up and is associated with sex, age, and H. pylori infection. Gastroscopy should be considered part of a routine health check.

The protective effects of rutaecarpine on acute pancreatitis.

Acute pancreatitis (AP) is the acute inflammation of the pancreas. The morbidity of AP has increased in recent years. Certain patients eventually develop severe AP (SAP), which rapidly progresses to multiple organ dysfunction; the incidence of this occurring in patients with AP is 20-30%. To date, no specific drugs or methods exist to treat this disease. Rutaecarpine relaxes vascular smooth muscle by stimulating calcitonin gene-related peptide (CGRP) release via activation of vanilloid receptor subtype 1 (VR1). It has been demonstrated that rutaecarpine induces a therapeutic effect on SAP. The present study was conducted to characterize the molecular mechanisms underlying the protective effects of rutaecarpine against AP using a rat model of AP. Gross pathological changes of the pancreas, as well as the pancreatic tissue histopathological score, were assessed following treatment with rutaecarpine, capsazepine or a combination of the two. Serum amylase activity was detected using an automatic biochemistry analyzer. Changes in the serum concentrations of interleukin (IL)-6, tumor necrosis factor (TNF-α), IL-10 and CGRP were assessed by ELISA and radioimmunoassay. The results demonstrated that pre-treatment with rutaecarpine markedly decreased pancreatic inflammation and necrosis, reduced the volume of ascites, and significantly increased the plasma concentration of CGRP and the serum concentration of IL-10, an anti-inflammatory cytokine. However, serum concentrations of the inflammatory cytokines IL-6 and TNF-α were decreased. The effect of rutaecarpine treatment markedly improved with increases in the drug dose. Capsazepine, as a competitive vanilloid receptor antagonist, abolished these protective effects of rutaecarpine against AP. Therefore, the results of the present study indicate that rutaecarpine protects against AP in rats by upregulating endogenous CGRP release via activation VR1 of, to improving the microcirculation of the pancreatic tissue and regulate the expression of inflammatory factors.

Cell motility and spreading promoted by CEACAM6 through cyclin D1/CDK4 in human pancreatic carcinoma.

Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) belongs to the human carcino-embryonic antigen (CEA) family. Numerous lines of studies have indicated that altered expression of CEACAM6 may have a role in carcinogenesis and development. However, few studies have defined functional roles and mechanisms of action. In the present study, the relationship between clinical and pathological parameters was also analyzed. The relative CEACAM6 protein expression of pancreatic carcinoma was significantly higher than that in non-cancerous tissue. Different clinical stages and lymph node metastasis between groups were significantly different (P<0.05). We used siRNA and forced-expression in multiple cell lines to define the role of CEACAM6 in the regulation of proliferation of pancreatic carcinoma in vitro and in vivo. Knockdown of endogenous CEACAM6 decreased proliferation of BxPC-3 and SW1990 cells. These changes significantly reduced cyclin D1 and CDK4 protein levels. Conversely, overexpression of CEACAM6 in MIA PaCa-2 cells stimulated proliferation and increased cyclin D1 and CDK4 protein levels. Our results confirm that CEACAM6 promoted cell proliferation, and these changes were mediated by cyclin D1/CDK4. These observations contribute to our understanding of the important roles of CEACAM6 in pancreatic carcinoma development and progression and could be a promising molecular target for the development of new diagnostic and therapeutic strategies of pancreatic carcinoma.