SUMMARYBackground: Probiotics are efficacious for treating and maintaining remission of ulcerative colitis. Aim: To conduct a randomized placebo-controlled trial of bifidobacteria-fermented milk supplementation as a dietary adjunct in treating active ulcerative colitis. Methods: Twenty patients with mild to moderate, active, ulcerative colitis randomly received 100 mL/day of bifidobacteria-fermented milk or placebo for 12 weeks with conventional treatment. Results: Clinical and endoscopic activity indices and histological scores were similar in the two groups before treatment. Although improvements were significant in both groups, the clinical activity index was significantly

AIM:To determine the anti-inflammatory activity of probiotic Bifidobacteria in Bifidobacteria-fermented milk (BFM) which is effective against active ulcerative colitis (UC) and exacerbations of UC, and to explore the immunoregulatory mechanisms. METHODS:Peripheral blood mononuclear cells (PBMNC) from UC patients or HT-29 cells were co-cultured with heat-killed probiotic bacteria or culture supernatant of Bifidobacterium breve strain Yakult (BbrY) or Bifidobacterium bifidum strain Yakult (BbiY) to estimate the amount of IL-10 or IL-8 secreted.RESULTS: Both strains of probiotic Bifidobacteria contained in the BFM induced IL-10 production in PBMNC from UC patients, though BbrY was more effective than BbiY. Conditioned medium (CM) and DNA of both strains inhibited IL-8 secretion in HT-29 cells stimulated with TNF-α, whereas no such effect was observed with heatkilled bacteria. The inhibitory effect of CM derived from BbiY was greater than that of CM derived from BbrY. DNAs of the two strains had a comparable inhibitory activity against the secretion of IL-8. CM of BbiY induced a repression of IL-8 gene expression with a higher expression of IκB-ζ mRNA 4 h after culture of HT-29 cells compared to that in the absence of CM. CONCLUSION:Probiotic Bifidobacterium strains in BFM enhance IL-10 production in PBMNC and inhibit IL-8 secretion in intestinal epithelial cells, suggesting that BFM has anti-inflammatory effects against ulcerative colitis.

The 2-week triple antibiotic therapy produced improvement, remission, and steroid withdrawal in active UC more effectively than a placebo.

INTRODUCTIONRecent studies have shown that re¯ux oesophagitis may develop after the successful treatment of Helicobacter pylori infection.1, 2 We and others have reported previously that H. pylori eradication causes an alteration in gastric acid secretion.3±8 Although gastric acid secretion has been accepted as a key factor in the pathogenesis of re¯ux oesophagitis, the relationship between changes in acid secretion and the development of re¯ux oesophagitis after H. pylori eradication is not well known. Recently, we have developed a convenient method for measuring stimulated gastric acid secretion. The method, named endoscopic gastrin test, can be performed in a short time concomitantly with the routine endoscopic examination.10 It has been con®rmed in a previous study that the results of the endoscopic gastrin test are highly reproducible and are correlated signi®-cantly with the peak acid output determined by the conventional gastric acid stimulation test. In the present study, using the endoscopic gastrin test, we investigated whether changes in gastric acid secretion after H. pylori eradication play a role in the development of re¯ux oesophagitis. In addition, we investigated the in¯uence of the presence or absence of hiatal hernia, an important pathogenic factor of re¯ux oesophagitis. 11±13 SUBJECTS AND METHODS SubjectsA total of 105 with H. pylori infection in whom re¯ux oesophagitis had been ruled out endoscopically (76 men and 29 women, mean age 51.5 years) were followed up SUMMARY Background: The role of acid secretion in re¯ux oesophagitis which may develop after H. pylori eradication is not well known. Aim: To investigate the participation of altered gastric acid secretion and the presence of hiatal hernia in the development of re¯ux oesophagitis after eradication therapy for H. pylori. Subjects and Methods: A total of 105 patients with H. pylori infection, but without re¯ux oesophagitis at the time of eradication therapy, were followed prospectively for 7 months after the clearance of this microorganism.

INTRODUCTIONIt has been shown that there are circadian variations in gastrointestinal function including gastric acid secretion, gastrointestinal motility, gastric mucosal blood flow, gastric epithelial cell turnover and gastric mucosal prostaglandin production. [1][2][3][4][5][6] With regard to circadian variation in gastric mucosal injury, Olson et al. 7 reported that acidified aspirin or absolute ethanol caused significantly more gastric mucosal lesions when administered in the light than in the dark phase. In contrast, Ventura et al. 8 reported that the highest acid secretory capacity and greatest degree of gastric mucosal damage produced by exogenously applied butyric acid was observed during the dark period in the rat gastric mucosa Ussing-chamber model. Waldrop et al. 9 demonstrated that significantly less severe ulcer formation occurred as a result of cervical spinal cord transection when rats developed the lesion at the onset of light (08.00 h) than at any other sample time. Thus, although rats show circadian variation in their susceptibility to gastric mucosal injury, results are variable among experimental models and conditions. The pineal gland secretory product, melatonin, is well known to have circadian and antistress SUMMARYBackground: We previously demonstrated the circadian variation of water-immersion restraint stress (WRS)-induced gastric mucosal lesions in rats. Aim: To investigate the roles of melatonin and prostaglandin in the gastric mucosa in circadian modulation of WRS. Methods: Fasted rats were subjected to 4-h WRS during both the diurnal and nocturnal phases of a light/dark cycle. Mucosal lesions, serum melatonin concentrations, mucosal generation of prostaglandin E 2 (PGE 2 ) and mucosal gene expressions of cyclooxygenase (COX)-1 and -2 were evaluated. Results: Lesion area after 4-h stress during the dark phase was significantly smaller than that in light-phase controls. Serum melatonin concentration in control rats during the light phase was significantly increased 4 h