We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4,655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100,000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. Despite a worldwide decline in incidence, gastric cancer remains one of the leading causes of cancer-related death in Japan. [1][2][3][4] There is a marked geographic variability in the gastric cancer incidence rate; the cancer is most common in China and Japan, and one of the lowest rates is in the United States. [1][2][3][4] Many epidemiologic studies have shown that the risk of gastric cancer is strongly associated with environmental factors, such as salt, nitrates and low intake of fresh fruits and vegetables. 1,4 -8 Recent studies have indicated that Helicobacter pylori infection is also a major risk factor for the development of gastric cancer. 9 -18 The prevalence of H. pylori infection is markedly higher in Japan than in other industrialized countries, although the reasons are not fully understood. 19 -21 The observed geographic variability in gastric cancer appears to be explained by a synergistic interaction between H. pylori infection and other environmental factors.The H. pylori bacterium colonizes the stomach mucosa and triggers a series of inflammatory reactions. It is considered an important cause of chronic atrophic gastritis (CAG), 19 -23 as shown in rodent models. 24 -26 CAG is considered the first step of a sequence of mucosal changes in the stomach leading to cancer. The current model for stomach carcinogenesis begins with gastritis, proceeds to CAG, then to intestinal metaplasia, dysplasia and, finally, carcinoma. 1,27 This hypothesis is supported by a considerable number of clinicopathological and epidemiological studies in countries with a high incidence of gastric cancer. However, longitudinal cohort studies that report an association of CAG with gastric cancer and a relation between the progression of CAG and the development of gastric cancer are limited. 28 -30 In addition, the role of H. pylori infection in the above-mentioned process of stomach carcinogenesis remains unclear. To investigate these problems relating to gastric cancer development, we established a cohort of male factory workers that we followed prospectively for 8 years.CAG in a high-risk population, such as Japanese subjects, usually begins at the gastric antrum and extends proximally towards the cardia. [31][32][33] As a result, gastric secretory function diminishes as the area of functional fundic gland mucosa gets smaller. 34 CAG is a histopathological diagnosis. It is difficult, howe...

Background: We have previously shown that the intraluminal concentration of NO in H. pylori‐positive patients is significantly reduced compared to that in H. pylori‐negative patients. Aim: The aim of this study was to evaluate the effect of H. pylori infection on gastric motor activity in relation to the level of NO and nitrite in the stomach in humans. Methods: Thirty‐two H. pylori‐negative and 32 H. pylori‐positive patients with dyspepsia were studied. Gastric myoelectrical activity was recorded for 24 h using surface electrogastrography. Intraluminal gas and juice were endoscopically collected from the stomach to determine NO and nitrite and nitrate (NOx) levels using a chemiluminescence system. Results: The percentage of tachygastria in the morning preprandial state was significantly higher (P=0.005) in H. pylori‐positive than ‐negative patients. In H. pylori‐negative patients, there was a significant positive correlation between NO levels and the percentage of bradygastria (r=0.56, P=0.001) and a significant negative correlation between NOx levels and the percentage of normal electrical activity (r=− 0.57, P=0.001) in the preprandial state. Conclusions Gastric motor activity is associated with NO and NOx levels in the gastric lumen. H. pylori infection may play a role in the pathogenesis of abnormal gastric myoelectrical activity.

The influence of neonatal thyroidectomy (Tx) on GH production was investigated by means of Northern blot analysis. Tx resulted in a significant decrease in pituitary GH mRNA levels after 10, 15 and 20 days. The changes of pituitary GH mRNA were soon reflected in pituitary GH content. There was, however, no significant difference in pituitary GH mRNA levels and GH content between Tx and sham-operated rats at 5 days old. The pituitary GH cells were significantly decreased in number 15 and 20 days after Tx. These data suggest that GH mRNA is transcribed, independent of thyroid hormone, in the rat anterior pituitary gland during early neonatal life. In addition, the present study ascertained that GH dependence on thyroid hormone is acquired between the 5th and 10th day of neonatal life.

Behçet's disease (BD) is a systemic inflammatory disease of unknown origin that affects various parts of the body. In some patients, the prognosis of the disease appears to be altered by the involvement of the intestine (intestinal BD). In intestinal BD, deep ulcers develop in the gastrointestinal tract, typically in the ileocaecum. Intestinal lesions in patients with BD are much more common in countries in the Far East, especially Japan. The tissue damage occurring in patients with BD is believed to be caused by oxygen radicals, which are promoted by proinflammatory cytokines and arachidonic acid metabolites. New formulations of mesalazine (5-aminosalicylic acid; 5-ASA) are now available for the treatment of intestinal BD. Mesalazine breaks the chain reaction of free radical production. Mesalazine may provide an effective treatment for the promotion of long term healing of mucosal ulceration of the intestine in patients with BD.

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