Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR-20b and miR-451a was determined in GC cell lines and the INS-GAS mouse model. Using Western Blot and luciferase reporter assay we determined that miR-20b directly regulates expression of PTEN and TXNIP, and miR-451a: CAV1 and TSC1. Loss-of-function experiments revealed that down-regulation of miR-20b and up-regulation of miR-451a expression exhibits an anti-tumor effect in vitro (miR-20b: reduced viability, colony formation, increased apoptosis rate, and miR-451a: reduced colony forming ability). To summarize, the present study identified that expression of miR-20b and miR-451a are deregulated in vitro and in vivo and have a tumor suppressive role in GC through regulation of the PI3K/AKT/mTOR signaling pathway.

Background: The aim of this study is to evaluate the role of NADPH oxidase in primary intestinal epithelial cells during the active phase of UC. Methods: The primary human colonic epithelial cells were isolated from 19 patients with mild to moderate inflammatory activity of UC and 14 controls using chelation method. The cells were cultivated under the effect of mediators. Viability of cells was assessed by fluorescent microscopy. Production of reactive oxygen species (ROS) by the cells was measured fluorimetrically using Amplex Red. Production of TNF-α cytokine by the colonic epithelial cells was analysed by ELISA. Results: The results of our study showed that unstimulated cells of UC patients had a decreased viability, increased ROS production, but similar TNF-α level when compared to the controls. Stimulation with LPS increased hydrogen peroxide and TNF-α level in the UC group. Treatment of colonic epithelial cells with NADPH oxidase inhibitor increased cell viability decreased the levels of ROS and TNF-α in the LPS-treated cells isolated from UC patients. Conclusions: Our study showed that bacterial endotoxins induced NADPH oxidase activation in the colonic epithelial cells. Moreover, we revealed that treatment with NADPH oxidase inhibitors had a protective effect against pro-inflammatory action of LPS in human colonic epithelium cells during inflammation.

Secretion of pepsinogen I (PgI), pepsinogen II (PgII), fasting gastrin-17 (fG-17) and stimulated gastrin-17 (sG-17) changes after Helicobacter pylori eradication. Few data are available on the long-term dynamics of gastric biomarkers after H. pylori eradication.The aim of this study was to investigate the dynamics of gastric biomarkers in H. pylori-positive patients after eradication over a 3-year period and to compare the levels with initially H. pylori-negative patients.Blood samples for the detection of gastric biomarkers were obtained from dyspeptic patients coming for upper gastrointestinal endoscopy. In H. pylori-positive patients, after eradication therapy, three follow-up blood samples were drawn after 12, 24 and 36 months; in H. pylori-negative patients, two samples were taken - at 12 and after 30 months. Median values of biomarkers in follow-up samples were compared with the baseline sample.The final sample included 110 patients (median age 67 years, M/F ratio 27/83). In patients after H. pylori eradication (n=83) PgI, PgII, fG-17 and sG-17 had decreased significantly during a 36-month period, whereas the PgI/PgII ratio had increased significantly from 5.59 to 11.64.In H. pylori-positive dyspeptic patients, after eradication therapy, a decrease in PgI, PgII, fG-17 and sG-17 was observed after 36 months whereas an increase in the PgI/II ratio suggested an improvement in gastric atrophy. The median levels of gastric biomarkers in patients after H. pylori eradication therapy may become similar to biomarker levels among initially H. pylori-negative individuals.

Objective. The aim of this study was to evaluate the incidence of inflammatory bowel disease in Kaunas and its region during a 3-year period. Material and Methods. The study was conducted during the 3-year period (2007–2009) and enrolled the patients from Kaunas with its region, which has a population of 381 300 inhabitants. The data were collected from all practices in the area where the diagnosis of inflammatory bowel disease was made by practicing gastroenterologists and consulting pediatricians along with endoscopists. Only new cases of inflammatory bowel disease were included into analysis. The diagnosis of ulcerative colitis and Crohn’s disease was strictly made according to the Copenhagen criteria. Age- and sex-standardized incidence was calculated for each year of the study period. Results. A total of 108 new inflammatory bowel disease cases were diagnosed during the study period: 87 had ulcerative colitis, 16 Crohn’s disease, and 5 indeterminate colitis. The incidence of ulcerative colitis, Crohn’s disease, and indeterminate colitis for each study year was 6.85, 5.33, and 7.38 per 100 000; 0.95, 1.11, and 1.57 per 100 000; and 0.47, 0.21, and 0.42 per 100 000, respectively. The average 3-year standardized incidence of ulcerative colitis, Crohn’s disease, and indeterminate colitis was 6.52, 1.21, and 0.37 per 100 000, respectively. The mean patients’ age at onset of ulcerative colitis, indeterminate colitis, and Crohn’s disease was 49.95 (SD, 17.03), 49.80 (SD, 17.71), and 34.94 years (SD, 0.37), respectively. Conclusions. The average 3-year incidence of ulcerative colitis in Kaunas region was found to be lower as compared with that in many parts of Central and Western Europe. The incidence of Crohn’s disease was low and very similar to other countries of Eastern Europe. Age at onset of the diseases appeared to be older than that reported in the Western industrialized countries.