AIM:To investigate glue extrusion after endoscopic N-butyl-2-cyanoacrylate injection on gastric variceal bleeding and to evaluate the long-term efficacy and safety of this therapy. METHODS:A total of 148 cirrhotic patients in our hospital with esophagogastric variceal bleeding (EGVB) were included in this study. N-butyl-2-cyanoacrylate was mixed with lipiodol in a 1:1 ratio and injected as a bolus of 1-3 mL according to variceal size. Patients underwent endoscopic follow-up the next week, fourth week, second month, fourth month, and seventh month after injection and then every 6 mo to determine the cast shape. An abdominal X-ray film and ultrasound or computed tomographic scan were also carried out in order to evaluate the time of variceal disappearance and complete extrusion of the cast. The average follow-up time was 13.1 mo. RESULTS:The instantaneous hemostatic rate was 96.2%. Early re-bleeding after injection in 9 cases (6.2%) was estimated from rejection of adhesive. Late re-bleeding occurred in 12 patients (8.1%) at 2-18 mo. The glue cast was extruded into the lumen within one month in 86.1% of patients and eliminated within one year. Light erosion was seen at the injection position and mucosa edema in the second week. The glue casts were extruded in 18 patients (12.1%) after one week and in 64 patients (42.8%) after two weeks. All kinds of glue clumping shapes and colors on endoscopic examination were observed in 127 patients (86.1%) within one month, including punctiform, globular, pillar and variform. Forty one patients (27.9%) had glue extrusion after 3 mo and 28 patients (28.9%) after six months. The extrusion time was not related to the injection volume of histoacryl. Obliteration was seen in 70.2% (104 cases) endoscopically. The main complication was re-bleeding resulting from extrusion. The prognosis of the patients depended on the severity of the underlying liver disease. CONCLUSION:Endoscopic injection of cyanoacrylate is highly effective for gastric varices bleeding. The glue clump shape is correlated with anatomic structure of vessels. The time of extrusion was not related to dosage of the glue.

TXNDC5 can promote the growth and proliferation of gastric cells. Silencing of TXNDC5 can restrain the growth and proliferation of gastric cancer cells. The gene can enhance the capability of invasion of gastric cancer cells. In some respects, TXNDC5 could be thought as a tumor-enhancing gene in gastric cancer.

The upregulation or mutation of C-MYC has been observed in gastric, colon, breast, and lung tumors and in Burkitt’s lymphoma. However, little is known about the role C-MYC plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of C-MYC on the growth, proliferation, apoptosis, invasion, and cell cycle of the gastric cancer cell line SGC7901 and the gastric cell line HFE145. C-MYC cDNA was subcloned into a constitutive vector PCDNA3.1 followed by transfection in normal gastric cell line HFE145 by using liposome. Then stable transfectants were selected and appraised. Specific inhibition of C-MYC was achieved using a vector-based siRNA system which was transfected in gastric cancer cell line SGC7901. The apoptosis and cell cycles of these clones were analyzed by using flow cytometric assay. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The invasion of these clones was analyzed by using cell migration assay. The C-MYC stable expression clones (HFE-Myc) and C-MYC RNAi cells (SGC-MR) were detected and compared with their control groups, respectively. HFE-Myc grew faster than HFE145 and HFE-PC (HFE145 transfected with PCDNA3.1 vector). SGC-MR1, 2 grew slower than SGC7901 and SGC-MS1, 2 (SGC7901 transfected with scrambled control duplexes). The cell counts of HFE-Myc in the third, fourth, fifth, sixth, and seventh days were significantly more than those of control groups (P < 0.05). Those of SGC-MR1, 2 in the fourth, fifth, sixth, and seventh days were significantly fewer than those of control groups (P < 0.05). Cell cycle analysis showed that proportions of HFE-Myc and SGC-MR cells in G0–G1 and G2–M were different significantly with their control groups, respectively (P < 0.05). The apoptosis rate of HFE-Myc was significantly higher than those of control groups (P < 0.05). Results of colony-forming assay showed that the colony formation rate of HFE-Myc was higher than those of control groups; otherwise, the rate of SGC-MR was lower than those of their control groups (P < 0.05). The results of cell migration assay showed that there were no significant differences between experimental groups and control groups (P > 0.05). In conclusion, C-MYC can promote the growth and proliferation of normal gastric cells, and knockdown of C-MYC can restrain the growth and proliferation of gastric cancer cells. It can induce cell apoptosis and help tumor cell maintain malignant phenotype. But it can have not a detectable influence on the ability of invasion of gastric cancer cells.

Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn’s disease (CD). The abnormality of inflammatory and immune responses in the intestine contributes to the pathogenesis and progression of IBD. Autophagy is a vital catabolic process in cells. Recent studies report that autophagy is highly involved in various kinds of diseases, especially inflammation-related diseases, such as IBD. In this review, the biological characteristics of autophagy and its role in IBD will be described and discussed based on recent literature. In addition, several therapies for IBD through modulating the inflammasome and intestinal microbiota taking advantage of autophagy regulation will be introduced. We aim to bring new insight in the exploration of mechanisms for IBD and development of novel therapeutic strategies against IBD.

Background/Aim:MicroRNAs (miRNAs) are a class of small noncoding RNAs acting as posttranscriptional gene expression regulators in many physiological and pathological conditions. MiR-155 is one kind of miRNAs that plays an important role in causing various diseases. However, the precise molecular mechanism of the ectopic expression of miR-155 in Helicobacter pylori infection remains poorly understood. Autophagy has recently been identified as an effective way to control the intracellular bacterium survival. In the present study, we demonstrate a novel role of miR-155 in regulating the autophagy-mediated anti-H. pylori response.Patients and Methods:Totally 86 H. pylori-positive patients together with 10 H. pylori-negative, healthy control subjects were included in the study. Correlation between immunohistochemical grades and miR-155 expression were determined. Molecular mechanism of miR-155 on regulation of autophagy and elimination of intracellular H. pylori were determined using the GES-1 cell model.Results:We found that overexpression of miR-155 by transfecting miR-155 mimics could significantly decrease the survival of intracellular H. pylori, and this process was through induction of autophagy. Furthermore, there was a significant correlation between miR-155 and immunohistochemical grades in H. pylori-positive patients, and miR-155 expression were decreased in the intestinal metaplasia group.Conclusions:The results have indicated that the miR-155 expression level plays a key role in immunity response against H. pylori and this might provide potential targets for the future treatment of H. pylori-related diseases.