Objective To evaluate the effects of pantoprazole on patients with upper gastrointestinal bleeding and its safety, as compared with omeprazole. Methods Ninety patients with non variceal upper gastrointestinal bleeding were randomly assigned to two groups. Sixty patients were in the group of pantoprazole, including 24 patients with gastric ulcer, 33 duodenal ulcer and 3 erosive gastritis; 30 patients were in the group of omeprazole, including 9 patients with gastric ulcer, 15 duodenal ulcer and 5 erosive gastritis.Treatment schemes:either pantoprazole or omeprazole 80 mg were added into 250 ml 5% glucose respectively and then infused intravenously. The clinical signs of the patients including the amout of bleeding were observed. Results After the treatment, the symptoms and sings improved significantly in both groups( P 0.05). Both the total effective rate of pantoprazole and omeprazole on upper gastrointestinal bleeding was 96.7%. The rates of side effects were 1.7% in pantoprazole group and 3.4% in omeprazole group. Conclusion Pantoprazole is also an effective and safe drug for the non variceal upper gastrointestinal bleeding.

By using antr-ras P21 mouse monoclonal (MoAb), SCI-Oncogema 1, the authors examined immunohistochemica! staining in pancreatc adeocarcinoma. The percentage of positive staining was 24/43 (558%). Furthermore it was indicated that the positive staining rate of antr-ras P21 MoAb was related to either histopathological grade or clinical stage. Upon statistical analysis of the correlation between the staining of anti-ras P21 and patient prognosis with Kaplan-Meier curve and Log-rant test, the positive staining cases showed comparatively better prognosis than the negative ones. Our study suggests that ras P21 expression may be important in the early stage of pancreatic carcinoma.

With the method of endoscopic ultrasonography (EUS) and Color scale ultrasound, 156 patients with stomach and gallbladder diseases were examined, The features revealed by the EUS and color scale ultrasound for these diseases were compared with the pathological changes. The findings were that:the mean color quantity scale of benign gastric ulcer was higher than that of gastric cancer(p<0.01).The gallbladder stone was two color quantity scales higher than did polypoid lesions of gallbtadder(p<0.01).The color scale ultrasound can improve the clear degree of lesion pictures.The correct rates of diagnosis were no significant differences between color scale ultrasound and grev scale ultrasound.

To investigate the distrbution of cag Ⅰin Helicobacter pylori(Hp) isolated from Chinese patients, and its relationship to gastroduodenal diseases. Fragment in cag Ⅰ was amplified by polymerase chain reaction(PCR) in 107 Hp strains from Chinese patients. Results The amplicom to cag Ⅰ was positive in 93 strains, of which 57 strains came from patients with chronic gastritis, 31 strains from peptic ulcer, and 5 strains from gastric carcinoma.Conclusion Existance of cag Ⅰ of Hp strains was popular in the Chinese population, but no data had proven the relation ship between the existence of cag 1and occurrence of Hp related diseases and inflammatory infiltration in gastric mucosa.

To investigate the distribution of IS605 in Helicobacter pylori(Hp) isolated from Chinese patients, and its relationship to gastroduodenal diseases. The fragment in IS605 was amplified by polymerase chain reaction(PCR) in 107 Hp strains from Chinese patients. Results: The amplicom to IS605 was positive in 47 strains. Detective rates of IS605 in Hp from duodenal ulcer (13.6%) were lower than that from gastritis(52.2%). It suggested that: the detection of IS605 was related to alternation in virulence of Hp.

To determine the role of GMBF in gastric mucosal tolerant cytoprotection under stress and its possible regulator, SD rats were exposed to repeated WRS, during which L NAME , a non selective NOS inhibitor, or L Arg, a substrate for NO synthesis, was administered to inhibit or promote the synthesis of NO, GMBF was measured using LDF 3 Flowmeter, NO level in gastric mucosa was monitored by Griess reaction, and gastric mucosal lesions were evaluated by UI. The results showed that gastric tolerant cytoprotection was accompanied by increased GMBF and NO level in gastric mucosa. Inhibition of endogenous NO synthesis by L NAME worsened mucosal lesions induced by WRS. After repeated WRS, adaptive increase of GMBF was abolished and NO content in gastric mucosa significantly reduced. In contrast, enhancement of endogenous NO synthesis by L Arg attenuated mucosal erosions produced by WRS and GMBF, NO content in mucosa increased. Good relationships between the changes in GMBF, UI, NO content in mucosa were found. It suggested that GMBF might play an important role in gastric mucosal tolerant cytoprotection. Endogenous NO might be one of its regulators. Inhibition of its synthesis delayed the induction of tolerant cytoprotection, while enhancementpromoted it.

The aim of the study is to evaluate the presence of mutations of p53 gene in RE and esophageal tumor induced by reflux of different gastro intestinal secretions. Gastroesophageal reflux(G), duodenoesophageal reflux(D) and duodeno gastroesophageal reflux(DG) model and control group(C) were reproduced by operations. All rats were given carcinogen (methyl n amyl nitrosamine) and their esophagi were harvested at 20, 26, 40 weeks after the operation. DNA was extracted and PCR amplification for 5, 6, 7, 8 exon of p53 followed by SSCP and AgNO 3 staining were used to detect mutation of p53 gene. It was showed that p53 gene mutations occurred in D and DG group at 20 weeks, and then more mutations were found at 26 and 40 weeks. The total rate of p53 mutation was 15 4% in groupc, 11 7% in G, 31 6% in D,and 33 3% in DG.The changes in the last two groups were significantly more compared with the former two groups.It is suggested that reflux of duodenal contents might promote mutations in p53 gene in esophageal mucosa, and reflux of gastric juice alone has lesser impact on p53 mutation.

A vector for a mutant Chinese Helicobacter pylori (Hp) strains knock out pathogenicity island (PAI) was constructed, which was the basis to establish a Chinese Hp mutant deleting pathogenicity island. Genetic engineering techniques such as polymerase chain reaction, plasmid extraction, agarose gel electrophoresis, restriction analysis, ligation, preparation of competence cell and transformation were used to make two cloning fragments containing two end regions of PAI and a selectable chloramphenicol resistance marker between them, and then engineering the recombined fragments into pBluescript plasmid. The result showed that restriction analysis demonstrated that the engineering mutant vector had been recombined. It suggested that we constructed an engineering mutant vector which targeted to delete the PAI in Chinese Hp strains. It will be useful for addressing the role of PAI in the pathogenesis of Hp infection.

The purpose of this study was to investigate clinical feasibility of treatment of pancreatic pseudocyst by endoscopy. We reported here one case of large pancreatic psuedocyst that was treated by endoscopic ultrasonography guided cystogastrostomy.The patient's symptoms resolved on the same day of operation. And one week later, the pancreatic pseudocyst decreased by more than 50% in size. Pancreatic psuedocyst resolved and didn't relapse after 6 months. So endoscopic ultrasonography guided cystogastrostomy is a safe, reliable, effective therapy for pancreatic pseudocyst with few complications.

The purpose of the present study was to assess the diagnostic value of endoscopic ultrasonography(EUS) and ERCP separately and their combination in chronic pancreatitis. There were 262 cases of chronic pancreatitis from January 1993 to May 2001 in our hospital. Among them 60 cases examined by ERCP and EUS were analyzed retrospectively. The constriction and dilatation of main pancreatic duct and pancreatic duct stones were found by EUS. In all, there were 49 patients who diagnosed chronic pancreatitis by EUS and the accuracy rate was 81 7%. On the other hand, there were 52 patients were diagnosed chronic pancreatitis by ERCP and the accuracy rate was 86 7%. There were also 6 patients who diagnosed by ERCP but undiagnosed by EUS, their coincidence rate was 90%. Furthermore, 59 patients were diagnosed by ERCP in combination with EUS and the accuracy rate was 98 3% ( vs sole ERCP or sole EUS respectively, P