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.

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.

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.

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

Objective To study the association of methylation status of C5 of the cytosine in the CpG di-nucleotide of caspase-8 promoter and expression of caspase-8 mRNA with the resistance to tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) in human hepatocellular carcinoma cell lines,and to evaluate the effect of demethylation agent 5-Aza-2′-deoxycytidine(5-Aza-CdR) on the resistance to TRAIL of human hepatocellular carcinoma cell lines.Methods Methylation status of caspase-8 promoter was measured with methylation-specific PCR method(MSP).Expression of caspase-8 mRNA was detected with RT-PCR.Apoptosis induced by TRAIL was observed by Acridine Orange/Ethidium Bromide(AO/EB) staining.Results Unmethylated status of caspase-8 promoter was found in both HepG2 and SMMC 7721 hepatocellular carcinoma cells.5-Aza-CdR neither up-regulated caspase-8 mRNA expression nor increased the sensitivity of hepatocellular carcinoma cells to TRAIL.Conclusion caspase-8 promoter methylation status and caspase-8 mRNA expression are not related to the resistance to TRAIL.5-Aza-CdR can not increase the sensitivity of hepatocellular carcinoma cells to TRAIL.

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.

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

The relationship between the intestinal metaplasia subtypes and the development of gastric carcinoma (GC) was. investigated with mucohistochemical staining on 576 biopsy specimens taken from patientswith intestinal metaplasia (IM) and 85 specimens taken from gastrointestinal mucosa of normal adults and fetus,IM was classified into 3 types, complete (type Ⅰ) and 2 classes of incomplete (types Ⅱ & Ⅲ) depending on the absence or presence of sulphomucin within the mucin secreting columnar cells. Type III IM was significantly more common in patients with GC and in those with dysplasia than in patients with benign gastric pa,tholgy(P

The expression of gastric carcinoma related antigen was observed in 110 gastrectomy specimens with gastric carcinoma and 343 biopsy specimens with intestinal metaplasia by ABC immunohistochemical staining with MG 7 , a monoclonal antibody against human gastric carcinoma. Intestinal metaplasia was classified into types I, II and III by histochemical mucin stainings. Among the 110 cases of gastric carcinomas, 92 (83.6%) showed the positive reaction for MG 7 related antigen. In different types of intestinal metaplasia, type III (46.7%) exhibited a significantly higher positive rate for MG 7 related antigen than type II (25.6%) and type I (18.6%) (P

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