Capsaicin is the major pungent ingredient in red peppers which is world widely consumed. Except its potent pain relieving efficacy as reported, capsaicin also exerted its antitumor activity in several tumor models. Here, we reported that capsaicin had a profound anti-proliferative effect on human colon cancer cells via inducing cell cycle G0/G1 phase arrest and apoptosis, which was associated with an increase of p21, Bax and cleaved PARP. The underlying mechanism of capsaicin's antitumor potency was mainly attributed to the stabilization and activation of p53. Capsaicin substantially prolonged the half-life of p53 and significantly elevated the transcriptional activity of p53. Through suppressing the interaction between p53 and MDM2, MDM2-mediated p53 ubiquitination was remarkably decreased after capsaicin treatment, which resulted in the stabilization and accumulation of p53. The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin's antitumor activity. In summary, our data suggested that capsaicin, or a related analogue, may have a role in the management of human colon cancer.

AIM:To assess the effects of intramuscular analgesics (morphine, Ap-237, pethidine and tramadol) on human Oddi's sphincter motility with choledochoscope manometry. METHODS:A total of 70 patients having T tubes after cholecystectomy and choledochotomy were assessed by choledochoscope manometry. They were randomly divided into morphine group, Ap-237 group, pethidine group and tramadol group. Basal pressure of Oddi's sphincter (BPOS), amplitude of phasic contractions (SOCA), frequency of phasic contractions (SOF), duration of phasic contractions (SOD), duodenal pressure (DP) and common bile duct pressure (CBDP) were scored and analyzed. All narcotic analgesic drugs were administered intramuscularly. RESULTS:Levels of BPOS, SOCA and SOF were increased after injection of morphine and Ap-237 (P<0.05), level of CBDP was increased from 4.97±3.87 mmHg to 8.62±7.43 mmHg (10 min later) and 7.32±5.95 mmHg (20 min later) after injection of morphine (P<0.01). No apparent change occurred after intramuscular injection of pethidine. Level of BPOS was increased from 7.01±5.50 mmHg to 2.87±2.78 mmHg 10 min after injection of tramadol and SOCA was decreased from 63.34±35.29 mmHg to 45.90±27.86 mmHg (10 min later,P<0.05) and 35.97±24.30 (20 min later,P<0.01) after administration of tramadol. CONCLUSION:All these findings indicate that Oddi's sphincter manometry via choledochoscope is a practical and new way to study the dynamics of Oddi' s sphincter. The regular dose of morphine and Ap-237 could increase BPOS, SOF and SOCA. Morphine could increase the level of CBDP, demonstrating an excitatory effect on the sphincter of Oddi. Pethidine had no effect on Oddi's sphincter motility. Tramadol shows an inhibitory effect on the motility of the sphincter of Oddi and decreases levels of BPOS and SOCA.

The regular dose of GTN, ISDN and PTN showed inhibitory effect on SO motility, morphine showed excitatory effect on SO while GTN, ISDN and PTN could antagonize the effect of morphine. Among the three nitroester drugs, the effect of ISDN on SO was most significant.

group (t = 5.254, 3.438 and 3.527, P < 0.001). SOD of the reflux group was shorter than the control group (t = 2.049, P < 0.05). The level of serum gastrin and plasma motilin of the reflux group was much lower than the control group (t = -2.230 and -2.235, P < 0.05). There was positive correlation between the level of plasma motilin and SOBP and between the level of serum gastrin and SOBP and CBDP. CONCLUSION: About 35.9% of the patients with a T tube after cholecystectomy and choledochotomy have duodenal-biliary reflux. Most of them have sphincter of Oddi hypomotility and the decreased level of plasma motilin and serum gastrin. The disorder of gastrointestinal hormone secretion may result in sphincter of Oddi dysfunction. There is a close relationship between sphincter of Oddi hypomotility and duodenal-biliary reflux. INTRODUCTIONEndoscopic sphincterotomy (EST) is an important surgery to treat choledocholithiasis. About 50% of the patients after EST had biliary gas indicating reflux of duodenal contents [1] . The duodenal-biliary reflux rate was as high as 100% in the patients after EST [2] . The stone recurrence rate was 9.8% in the patients with EST [3] , but in the patients after cholecystectomy for gallbladder stones, the choledocholithiasis recurrence rate was only about 2.5% [4] . Thus, EST destroyed the sphincter of Oddi, resulting in duodenal-biliary reflux which may have close relationship with the recurrence of choledocholithiasis. Abstract AIM: To detect whether patients with a T tube after cholecystectomy and choledochotomy have duodenalbiliary reflux by measuring the radioactivity of Tc99m-labeled diethylene triamine penta-acetic acid (DTPA) in the bile and whether the patients with duodenal-biliary reflux have sphincter of Oddi hypomotility, by measuring the level of plasma and serum gastrin of the patients. Finally to if there is close relationship among sphincter of Oddi hypomotility, duodenal-biliary reflux and gastrointestinal peptides. METHODS: Forty-five patients with a T tube after cholecystectomy and choledochotomy were divided into reflux group and control group. The level of plasma and serum gastrin of the patients and of 12 healthy volunteers were measured by radioimmunoassay. Thirty-four were selected randomly to undergo choledochoscope manometry. Sphincter of Oddi basal pressure (SOBP), amplitude (SOCA), frequency of contractions (SOF), duration of contractions (SOD), duodenal pressure (DP) and common bile duct pressure (CBDP) were scored and analyzed. RESULTS: Sixteen (35.6%) patients were detected to have duodenal-biliary reflux. SOBP, SOCA and CBDP in the reflux group were much lower than the control

The formation of pigment gallstone was related to the abnormal function of the intestinal mucosal barrier. The abnormality in the function of the intestinal mucosal barrier probably induced the formation of gallstone by a bacterial translocation mechanism.