DNA Methylation ; Helicobacter Infections ; complications ; Helicobacter pylori ; Humans ; Stomach Neoplasms ; etiology ; genetics ; Telomerase ; physiology

Objective To investigate whether a novel mucosal adjuvant (DNA containing six base pair motifs consisting of an unmethylated CpG dinucleotide flanked by two 5′ purines and two 3′ pyrimidines, CpG Oligodeoxynucleotide, CpG ODN),which has not been shown to have significant toxicity,could be an ideal mucosal adjuvant for the development of a H. pylori vaccine in mice model. Methods C57BL/6 mice were orally or intranasally immunized with H. pylori whole cell sonicate(WCS) / cholera toxin (CT) or WCS /CpG ODN, and the corresponding control groups were set. Mice were dosed once a week for four weeks. One week after the last immunization, all animals were challenged by live H. pylori (5?10 8) three times in a five day duration. Two and 8 weeks after the last challenge, all animals were sacrificed to examine infection of H. pylori. Sera, saliva, gastric juice were collected to measure the concentrations of IgG, IgG1, IgG2a and IgA by ELISA. Results The protecting rates against H. pylori infection were 75%(9/12), 70% (7/10) and 0 (0/10) in the group of WCS/CT orally, WCS/CpG ODN intranasally and WCS/CpG ODN orally, respectively. Significantly higher levels of serum IgG2a antibody was found in the group immunized with WCS plus CpG ODN than those found in the sham immunized controls ( P

Objective To compare the detection rates of capsule endoseopies with push endoseo-pies. Methods From May 2002 through January 2003 , thirty - nine patients with suspected small bowel diseases, particularly the gastrointestinal bleeding of unknown origin were examined by capsule endoscopies. Of the 39 patients. 32 complained of obscure recurrent gastrointestinal bleeding. From January 1993 to October 1996, 36 patients suffered from unexplained GI bleeding underwent push endoscopies. All patients had prior normal results on gastroseopy, colonoscopy, small bowel barium radiography, seintigraphy and/ or angiogra-phy. Results M2A capsule endoscopies disclosed abnormal small bowel findings in 26 out of 32 patients (81% ). Twenty one of 26 patients had significant pathological findings in explaining their clinical disorders with diagnostic yield of 66% (21 of 32 patients). Definite bleeding sites diagnosed by capsule endoscopies in 21 patients including angiodysplasia 8, inflammatory small bowel diseases 5, small bowel polyps 4, GI stro-mal tumor 2,earcinoid tumor and lipoma 1 , and bemorrhagie gastritis 1. Push endoscopies detected the definite sources of bleeding in 9 of 36 patients (25%). Definite bleeding sources included angiodysplasia 2, leiomyosareoma 2, leiomyoma 1 , lymphoma 1 , Grohns disease 1 , small bowel polyps 1 ,and adenocareinoma of ampulla 1. Suspected bleeding sources were seen with push endoscopies in two additional patients, and other five patients with capsule endoscopies. Conclusion Gapsule endoseopy is superior to push endoscopy in detecting obscure GI bleeding ( P

Objective To investigate the main causes and strategies for the difficulties in ureteroscopic lithotripsy.Methods From March 2004 to December 2006,19 cases of ureteral calculi,who experienced difficulties during holmium laser lithotripsy or pneumatic lithotripsy under a rigid ureteroscope,were analyzed retrospectively.Among the cases,3 had difficulties in ureteroscope placement due to the narrow ureteral ingress,6 owing to calculus obstruction complicated with ureteral inflammatory polypi,4 resulted from twisted ureter,and 6 because of stenosis of the ureter.Results In 15 of the patients,the operation was successfully performed by changing surgical approach,controlling the hydraulic irrigation,and incising the stenotic segments,etc.Two patients,who had stenotic ureter,received ESWL with double-J catheter dwelling.Lithotripsy failed in 2 cases,and PCNL was used to remove the calculi.The postoperative complications occurred in 4 cases,including 2 with mucosal laceration and 2 ureteral perforations.One of the 4 cases was transferred to an open surgery,and the other 3 were cured by conservative treatments.Conclusions Holmium Laser lithotripsy and pneumatic lithotripsy under a rigid ureteroscope are safe and effective in treating ureteral calculi.

Objective To investigate the molecular mechanism of Helicobacter pylori (H.pylori) resistance to clarithromycin. Methods The E test was used to determine clarithromycin resistant strains of H.pylori , and PCR Restriction Fragment Length Polymorphism (RFLP) analysis for 23S rRNA domain V gene mutations. Results Of nine clarithromycin resistant stains of H.pylori , including six primary and three acquired resistant strains, eight were found to have an A to G mutation in 23S rRNA domain V at position 2144. Conclusions The results indicated that the majority (88.8%) of clarithromycin resistant isolates of H.pylori in Shanghai have an A2144G mutation in 23S rRNA domain V.

Objective Atrophic gastritis, as a pre-cancerous condition of gastric cancer, is developed from non-atrophic gastritis.The aims of this study was to compare the gene expression profiles between atrophic gastritis and non-atrophic gastritis using cDNA microarray and to explore the molecular mechanisms in the development of atrophic gastritis. Methods Endoscopy and biopsy were performed consecutively in 227 patients (143 male, 84 female, age range between 16-72 years, with average age 48.6 years). Diagnosis of non-atrophic gastritis and atrophic gastritis was made according to histological examination, and 120 patients were in non-atrophic group and 107 in atrophic group. The total RNA was extracted from the biopsy specimens of two groups with Trizol reagent. cDNA microarray consisting 8 464 human genes (HGEC-80s kit) was used, and labeled cDNA with fluorescence probes were hybridized to microarray, and then the comparison of gene expression profiles was made between atrophic and non-atrophic gastritis. Results It was identified that in gene expression profiles of atrophic gastritis there were 165 genes showing a greater than 2-fold increase and 460 genes showing a greater than 50% decrease as compared to non-atrophic gastritis. RT-PCR analysis revealed similar results as in DNA microarray. Conclusions There is different expression in many genes between the gastric mucosal cells of non-atrophic and atrophic gastritis mucosa. Many genes expression profiles are involved in atrophic gastritis that would be of help in further understanding the development of atrophic gastritis.

Objective To evaluate the effectiveness of wireless capsule endoscopies in patients with suspected CD of the small bowel.Methods From May 2002 through April 2003, we prospectively examined 20 suspected CD patients by capsule endoscopies with normal results in other conventional examinations. It includes the presence of the following symptoms and signs: abdominal pain, weight loss, positive fecal occult blood test, iron deficiency anemia, diarrhea and fever. Mean duration of symptoms before diagnosis was 6 5 years.Results Of the 20 participants, 13 (65%) were diagnosed as having CD of the small bowel according to the findings of the M2A Given Capsule. Among the findings detected by the capsule were mucosal erosions (2 patients), aphthae (5 patients), granulomatous nodularity (1 patient), large ulcers (2 patients), and ulceration with incomplete obstruction (3 patients). All of the 13 patients who received medications showed good clinical improvement.Conclusion Wireless capsule endoscopies were the effective device for diagnosing patients with suspected CD, undetected by conventional diagnostic measures.It may be more likely to detect early lesions in the small bowel of patients with CD.

OBJECTIVETo investigate the therapeutic effect of retroviral endostatin gene transfer on the human colon cancer cell line, LoVo.

METHODSA retroviral vector pLESSN expressing secretable endostatin was constructed and packaged with a titer of 8.2 x 10(5) CFU/ml. A LoVo cell line was subjected to retrovirus-mediated endostatin gene transfer. The proviral integration of endostatin was analyzed with PCR. The function of endostatin was tested by MTT assay in vitro and a mouse xenograft model in vivo.

RESULTSAfter transfection and superinfection, amphotropic retrovirus was collected, and transduction with amphotropic retroviruses resulted in endostatin proviral integration. The endostatin secreted by transduced LoVo cells markedly inhibited cell growth up to 67% (P<0.001), compared with the control cells. The gene expression of endostatin in LoVo colon tumor cells significantly inhibited tumor growth in vivo. There was an 86% reduction in tumor size in the endostatin-transduced group, accompanied by a reduction in vessels, compared with the control group (P<0.01).

CONCLUSIONRetroviruses can allow functional expression of the endostatin gene in human colon tumors, showing promise for an antitumor strategy using antiangiogenesis.

Cell Division ; Cell Line, Tumor ; Colonic Neoplasms ; pathology ; therapy ; Endostatins ; genetics ; Gene Transfer Techniques ; Genetic Vectors ; Humans ; Retroviridae

To investigate the effects of low dosage of nitric oxide synthase (NOS) inhibitor Nc-nitro -L-arginine methyl ester ( L-NAME) in two-week treatment on the hyperdynamic circulatory state in rats with cirrhosis. METHODS: Cirrhosis model was induced in male SD rats by injection of 60 % CCL4 oily solution subcutaneously. Cirrhotic rats were treated with L-NAME ( 0.5 mg·kg-1·d-1) by gavage for two weeks. Mean arterial pressure ( AP ), portal pressure(PP), cardiac output ( CO ), cardiac index ( CI ), splanchnic vascular resistance ( SVR ), splanchnic blood flow(SBF) and serum nitrite levels were determined in L-NAME-treated, L-NAME-untreated cirrhotic rats and controls by using 57Co-labled microsphere technique and a fluorometric assay, respectively. RESULTS: Untreated cirrhotic rats had significantly lower MAP, SVR and higher PP, CO, CI, SBF and nitrite concentration than those of the controls (all,P< 0.01 ). In treated cirrhotic rats, L-NAME significantly attenuated the increase of CO, CI, SBF, nitrite concentration and the decrease of MAP and SVR. In treated cirrhotic rats, L-NAME induced a marked decrease of nitrite concentration than untreated cirrhotic rats[(1.471±0.907)μmol/L vs (4.204±1.253) μmol/L, P<0.01]. CONCLUSION: The endogenous NO may play an important role in the changes of hemodynamics pattern in cirrhosis, and hyperdynamic circulatory state in rats with cirrhosis can be ameliorated by oral two-week administration of lower dose of L-NAME.

Objective To investigate the interactions and effects of Helicobacter pylori (H.pylori) and non steroidal anti inflammatory drugs (NSAID) on the proliferation of gastric epithelial cells in vitro. Methods After co culturing of gastric cancer cell line AGS cells with H.pylori and/or NSAID (indomethacin and aspirin) for 48 hours, the cell proliferation and proliferating cell nuclear antigen (PCNA) were examined by MTT assay and Western blot. Results cagA positive H.pylori strain NCTC11637, but not cagA negative H.pylori strain NCTC12908, had the effect of enhancing gastric epithelium cell proliferation. However, the effect of proliferation was dependent on the density of H.pylori . It was demonstrated that low density (range from 3.2?10 4 CFU/ml to 4?10 6 CFU/ml) of bacteria suspensions resulted in proliferative effect, while high density (more than 2?10 7 CFU/ml) resulted in inhibition. Besides, indomethacin and aspirin inhibited cell proliferation in a dose dependent manner. Moreover, when AGS cells were incubated with cagA positive H.pylori and NSAID, inhibition rather than proliferation was observed. cagA positive H.pylori strains up regulated the expression of PCNA while indomethacin and aspirin down regulated the level of PCNA expression. Meanwhile, the expression of PCNA was also reduced significantly when AGS was co cultured with H.pylori and NSAID. Conclusions The results indicated that gastric epithelium cell proliferation was associated with different H.pylori strains and its density. cagA positive H.pylori strain is prone to increase cell proliferation, but cagA negative H.pylori strain has no such effect. NSAID can inhibit gastric epithelial cell proliferation and reverse such effect caused by H.pylori.