Gastric cancer develops in persons infected with H. pylori but not in uninfected persons. Those with histologic findings of severe gastric atrophy, corpus-predominant gastritis, or intestinal metaplasia are at increased risk. Persons with H. pylori infection and nonulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps are also at risk, but those with duodenal ulcers are not.

Since the discovery of Helicobacter pylori in 1983, the concept of gastritis has greatly changed, with increasing interest focused on histological gastritis. 1 Many studies have shown that H. pylori infection causes histological gastritis, with persistent infection leading to atrophic gastritis. 2,3 Recent studies showing that differences in the strain of H. pylori, the timing of H. pylori infection and immunity of the host contribute to the degree of atrophic gastritis, have attracted considerable attention but remain controversial. 4±6 Among other factors, gastric secretory function can greatly affect the location of H. pylori-induced gastritis. 7 In patients with duodenal ulcer who have excessive acid secretion, a high H. pylori density and histological gastritis are found primarily in the antrum; the H. pylori density is low in SUMMARY Background: Several studies have shown that acidsuppressive therapy aggravates corpus gastritis in patients with Helicobacter pylori infection, promoting the development of atrophic gastritis. Aim: To study the effects of long-term use of antisecretory agents on the H. pylori-positive gastric mucosa in Japan, a country with a high incidence of gastric cancer. Methods: A total of 141 H. pylori-positive patients who had peptic ulcers or re¯ux oesophagitis were treated for 3 years with either omeprazole (20 mg/day) alone (n 7) or with omeprazole for primary therapy (8 weeks), followed by famotidine (40 mg/day) for maintenance therapy (n 134). Endoscopy was performed before, during, and after treatment. Biopsy specimens were taken from the greater curvature of the antrum and corpus and were examined histologically.

Abstract.Although metastasis or relapse is a leading cause of death for patients with gastric cancer, the hematogenous spread of cancer cells remains undetected at the time of initial therapy. The development of novel diagnostic molecular marker(s) to detect circulating gastric cancer cells is an issue of great clinical importance. We obtained peripheral blood samples from 10 patients with gastric cancer who underwent laparotomy and 4 healthy volunteers. Microarray analysis consisting of 30,000 genes or ESTs was carried out using eight gastric cancer tissues and normal gastric mucosae. We selected 53 genes up-regulated in gastric cancer compared to normal gastric mucosae from our microarray data set, and, among these, identified five candidate marker genes (TSPAN8, EPCAM, MMP12, MMP7 and REG3A) which were not expressed in peripheral blood mononuclear cells (PBMCs) from 4 healthy volunteers. We further carried out semi-quantitative nested reverse transcription-polymerase chain reaction (RT-PCR) for HRH1, EGFR, CK20 and CEA in addition to the five newly identified genes using PBMCs of patients with gastric cancer, and found that expression of one or more genes out of the nine was detected in 80% of the patients with gastric cancer. Moreover, the numbers of genes expressed in PBMCs were ≤2 and ≥2 in all vascular invasion-negative cases and in 5 of 6 positive cases, respectively, showing significant differences between the two groups (P=0.041). Nested RT-PCR analysis for the set of nine marker genes using PBMCs may provide the potential for detection of circulating gastric cancer cells prior to metastasis formation in other organs.

A new enzyme‐linked immunosorbent assay (ELISA) for detecting the antibody to a human T‐lymphotropic virus type I (HTLV‐I) tax gene product, p40tax, has been developed. By this ELISA method, we have investigated the relationship between the presence of p40tax antibody in HTLV‐I‐infected mothers and the virus transmission rate from mothers to their children. The rate of mother‐to‐child transmission of HTLV‐I was higher in P40tax antibody‐positive mothers than in antibody‐negative ones. Thus, the presence of P40tax antibody may indicate an increased risk of vertical transmission of HTLV‐I.

ABSTRACT:The effect of LiClO 4 on the polymerization of methyl methacrylate (MMA) with dimethyl 2,2-azobisisobutyrate (MAIB) was investigated at 50ЊC in methyl ethyl ketone. The polymerization proceeded homogeneously even at [LiClO 4