for the China Gastric Cancer Study Group T HE ASSOCIATION BETWEEN chronic Helicobacter pylori infection and development of gastric cancer is well established. [1][2][3][4] The International Agency for Research on Cancer has categorized H pylori as a group I carcinogen. 5 In Correa's model of gastric carcinogenesis, the gastric mucosa progresses through the stages of chronic active gastritis, glandular atrophy, intestinal metaplasia, and dysplasia before the development of gastric adenocarcinoma. 6-10 Two recent large-scale, prospective studies, 11,12 both in high-risk populations, have re-ported H pylori infection as a definite risk factor for the development of gastric cancer. In the first study, presence of H pylori at baseline was associated with an increased risk of progression to dyspla-Author Affiliations and Members of the China Gastric Cancer Study Group are listed at the end of this article.

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1In 13 of 15 experiments, prostaglandin E2 (PGE2) and sulprostone (a prostanoid EPI/EP3-receptor agonist) contracted isolated rings of human pulmonary artery at low concentrations () 5 and > 0.5 nM respectively). Tissue was obtained from patients undergoing surgery mainly for carcinoma of the lung. Characterization of the receptors involved was complicated by loss of sensitivity to the contractile PGE action over the experimental period. In contrast, contractile responses to KCI, phenylephrine and the specific thromboxane (TP-) receptor agonist, U-46619, did not decrease with time. 2 The relative contractile potencies for seven PGE analogues, measured during the first few hours after setting up the preparations, were as follows: sulprostone > misoprostol = gemeprost > PGE2 > GR 63799X> 17-phenyl-w-trinor PGE2 1 1 1-deoxy PGE1. This ranking indicates that an EP3-receptor is involved. 3 The contractile action of sulprostone was not blocked by the TP-receptor antagonists, EP 169 and GR 32191, and the EPI-receptor antagonist, AH 6809.4 In two experiments, PGE2 (50 nM) reduced basal tone and sulprostone was a weak contractile agent.Phenylephrine-induced tone was also inhibited by PGE2 (EC50 = 5-20 nM), 1 1-deoxy PGEI and butaprost (a selective EP2-receptor agonist); the latter prostanoids were about 2 and 4 times less potent than PGE2 respectively. Interactions with phenylephrine were different in experiments where PGE2 alone was contractile: PGE2 induced contraction superimposed on the phenylephrine response and 11-deoxy PGE, induced either further contraction or had no effect. Butaprost produced relaxation at high concentrations; this may not be an EP2 action since preparations were highly sensitive to relaxant actions of prostacyclin (IP-) receptor agonists (cicaprost and TEI-9063). 5 The study has shown that in the majority of experiments on the human isolated pulmonary artery, the contractile EP3 system outweighed the relaxant EP2 system. However, in two experiments the reverse was true. It is not clear to what extent these differences are due to disease processes affecting the tissues. The findings are discussed in relation to the adverse cardiovascular responses occasionally encountered during treatment of postpartum haemorrhage with sulprostone, and more generally to the clinical use of EP-receptor agonists in man.