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.

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.

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 effects of ?-tocopheryl succinate (?-TOS) on apoptosis of gastric cancer cells induced by TRAIL. Methods The cell cycles and the percentage of apoptosis were analyzed with flow cytometer and the expressions of NF-?B, survivin, bcl-2 and caspase-3 in gastric cancer cells were assessed with Western blot. Results After being exposed to TRAIL 300ng/ml for 24 hours, the apoptosis rate was 36.05% for MKN28 and 11.80% for SGC-7901. When exposed to ?-TOS at 60?mol/L for 24 hours, the apoptosis rate was 9.0% for MKN28 and 8.5% for SGC-7901. With a combination of ?-TOS 60?mol/L and TRAIL 300ng/ml for 24 hours, the apoptosis rate was elevated to 48.1% for SGC-7901 and 63.7% in MKN28, respectively. The results of Western blot showed that TRAIL inhibited the expressions of NF-?B and survivin, while had no inhibition on the expressions of bcl-2 of SGC-7901 and MKN28 cell lines. The expression levels of bcl-2 and survivin had no change when the cells were exposed to ?-TOS alone. When the cells were treated with ?-TOS and TRAIL simultaneously, the expressions of NF-?B, bcl-2, and survivin were greatly decreased. Conclusions ?-TOS can enhance the activity of TRAIL in inducing apoptosis, and the down-regulation of the expression of NF-?B, bcl-2 and survivin may be involved in the mechanisms.

Objective To study the effects of concentrated H.pylori culture supernatant(CHCS) on the expressions of COXⅠ mRNA and protein in gastric carcinoma cells,and explore the potential role of H.pylori in the gastric carcinogenesis.Methods After SGC7901 cells were treated by 6 ?l/ml CHCS for 4 h,8 h,12 h respectively,the expression of COXⅠmRNA and protein was detected by RT-PCR and Western blotting.Results The expression of COXⅠmRNA decreased gradually after exposure to CHCS for 4 h.Especially after 8 h,the expression decreased significantly.When treated with CHCS for 12 h,the expression continued to decrease(P

Objective To explore the existing molecular pattern of rodent Muc3 carboxyl-terminal domain. Methods Muc3 carboxyl-terminal domain was expressed by a transient expression system and detected with SDS/PAGE and Western blotting. Identification of interaction between two proteolytically cleaved fragments was carried out by using both metabolic labeling and immunoprecipitation of expressed proteins and affinity purification of His-tagged proteins. Results Experiments with heterologous cells transfected with cDNA encoding the 381-residue C-terminal domain of rodent Muc3 showed that a definitive proteolytic cleavage occurred during the process in the endoplasmic reticulum. The products consisted of a V5-tagged 30 000 extracellular peptide, a Myc-tagged 49 000 membrane-associated peptide and non-cleaved 55 000 of whole-length protein. Two fragments remained associated by non-covalent SDS-sensitive interactions. Conclusion The proteolytic cleavage may be a prelude to later release of the large extracellular domains at cell surfaces. But the interaction between two cleaved fragments may be an important factor to interfere with the later release of the extracellular domain.

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