Helicobacter pylori ( H.pylori )infection is an important aetiological risk factor of gastric cancer, and has been classified as group I or definite carcinogen by the World Health Organization. The molecular mechanism of H.pylori leading to gastric cancer is still unclear. It has been increasingly recognized that cell proliferation and appoptosis,telomerase activition, genetic instability and abnormal DNA methylation are involved in the development of H.pylori related gastric cancer and its precursors. To better understand the pathogenesis of gastric cancer, a revie of the role of H.pylori infections in the induction of molecular events in gastric epithelial cells is presented in this paper.

Gastric cancer is a result of interaction of multiple factors. In previous studies it was found that genetic instability, abnormality of DNA methylation, telomere loss, mismatch of repair gene and k-ras mutation, loss of heterozygosity (LOH) of some of cancer-inhibitory genes such as APC, MCC and DCC, disbalance between cell proliferation and apoptosis, etc. were associated with the development of gastric cancer. It was also discovered that tretinoin, sodium selenite, sodium butyrate and epigallocatechin-3-gallate (EGCG) may be effective in preventing gastric carcinoma and gene therapy may partially reverse the malignant phenotype of gastric cancer cells.

In recent years, gastrointestinal pace-maker or electrical stimulation has been proposed as a therapeutic option. The interstitial cells of Cajal (ICC) are the pacemaker cells in the gastrointestinal tract.They have special properties that make them unique in their ability to generate and propagate slow waves in gastrointestinal muscles which determine the frequency, the direction and velocity of the propagation of peristaltic activity, in concert with the enteric nervous system for GI motility. Gastrointestinal pacing has been used in the treatment of gastroparesis syndrome, morbid obesity, irritable bowel syndrome, functional dyspepsia and gastroesophageal reflux disease. To better understand the gastrointestinal pacing, a review of its effects and mechanism is presented in this series of papers.

0 05). Conclusion mtMSI may be involved in the carcinogenesis of some hepatocellular carcinomas, but mtMSI is not associated with nMSI.

Objective It has been known that the C-terminal domain of rodent Muc3 underwent proteolytic digestion.G/S within the motif of cleavage,LSKGSIVV,was one of the important pivots for digestion.The present investigation was aiming at exploring the unknown relationship between the integrity of SEA module and the proteolytic digestion.Method Truncated rodent Muc3 C-terminal domains(p20t and p20SEA) were produced by site-directed mutagenesis to insert a stop code in the required place.Proteins were detected by SDS/PAGE and Western blotting.Deglycosylation of the expressed protein was performed by digestion using N-glycosidase F.Results Muc3 C-terminal domain was posttranslationally cleaved to produce a V5-tagged 30kDa extracellular glycopeptide and a Myc-tagged 49kDa membrane-associated glycopeptide.The 30kDa N-terminal fragment shifted to 22kDa after deglycosylation.The truncated rodent Muc3 C-terminal domain containing complete SEA module,but without the following residues after SEA module,was 30kDa Mw as detected with anti-V5 antibody,and it was shifted to 22kDa after deglycosylation.But the truncated rodent Muc3 C-terminal domain containing incomplete SEA module(p20t) of 26-30kDa Mw was shifted to 26kDa after deglycosylation.Conclusion There was proteolytic digestion in both complete rodent C-terminal domain and complete SEA module without residues after SEA module.But proteolytic digestion does not occur in the incomplete SEA module of rodent Muc3.So it may be concluded that the integrity of SEA module of rodent Muc3 was also a crucial condition for its proteolytic digestion.

Quantitative DNA measurements were done in mitotic figures in cells from early gastric carcinoma of intestinal type(n = 8), slight (n=10), moderate (n=10) and severe dysplasia (n = 8), and simple intestinal metaplasia (n=10). The mean DNA values were found to increase gradually from intestinal metaplasia to early gastric carcinoma, with the sequence of from slight, moderate to severe dysplasia, and the differences between each two adjacent groups being statistically signi ficant (P

The expression of tumor-associated glycoprotein (TAG-72) identified by monoclonal antibody B72.3 was investigated in HO resected specimens of gastric carcinoma,36 biopsied specimens of dysplasia,and 303 specimens of intestinal metaplasia(IM).IM was subdivided into complete Type I and incomplete Types Ⅱ and Ⅲ based on whether sulphomucin is present or absent in the mucin secreting columnar cells.The positive rate of TAG-72 in gastric carcinoma was 60.9%,and it was significantly higher in IM specimens with gastric carcinoma than in those with benign gastric lesions (P

005) The prevalence of Hp infection in antrum was significantly lower in patients with GERD (16/50) and BE (33/106) than that in control subjects (30/50,P

Objective To investigate the effect of membrane-cytoskelet on linker Ezrin in the invasion and migration of human adenocarcinoma cells line AGS. Methods Two small hair RNA targeting Villin2 gene ( Ezrin coding gene) was designed,chemically synthesized and inserted into plasmid pGenesil-shRNA,then transformed into E. coli DH5 ?. The recombinant plasmid was extracted in middle quantity and transfected into AGS cells by LipofectamineTM 2000. Ezrin expression in AGS cells transfected by shRNA recombinant plasmid was measured by RT-PCR and Western blotting. AGS cells were transfected by effective shRNA plasmid and cultured in 1640 media containing G418 ( 800 ?g/ml) . RT-PCR and Western blotting were applied respectively to detect the Ezrin mRNA and protein expression to evaluate the blocking effect of shRNA-Ezrin. Cell migration and invasion was determined by scratch test and Transwell chamber assay. Results Our designed shRNA knocked down 93% Ezrin in AGS cells which had a stable expression of Ezrin small hairpin RNAs. The migrated cells number of Ezrin knocked-down group was 27. 67 ? 4. 50,which was significantly decreased compared with the control group ( 125. 50 ? 8. 33,P

Objective To study of relationship of the mRNA expression of protection of telomeres 1(POT1) and the activity of telomerase with the incidence of gastric carcinoma.Methods Lesioned gastric mucosal tissues and the corresponding normal tissues from 30 cases of gastric cancer,30 cases of moderate or severe atypical hyperplasia,and 30 cases of intestinal metaplasia were collected in this study.The expression of POT1 mRNA was detected with real time-PCR and the activity of telomerase was examed with TRAP-ELISA.Results Real time-PCR analysis showed that POT1 expression was increased in the gastric carcinoma tissues compared with the paracancerous normal mucosal tissues,increased in the severe atypical hyperplasia than in the corresponding normal tissues,but there was no difference between intestinal metaplasia tissues and normal tissues.The activity of telomerase in the advanced gastric tumors and severe atypical hyperplasia was significantly higher than that in intestinal metaplasia tissues and normal gastric mucosal tissues.However no obvious difference was found in the activity in gastric tumors and severe atypical hyperplasia with intestinal metaplasia tissues and normal gastric mucosal tissues.Conclusion Although the activity of telomerase in gastric cancer and severe atypical hyperplasia is significantly higher than that in normal and intestinal metaplasia tissues,POT1 mRNA has no relationship with this change.