81.   Prostaglandins are well recognised as protecting the gastric mucosa and enhancing the perception of pain.

82.   Inhibition of prostaglandin synthesis by NSAIDs is the major established mechanism by which NSAIDs render the gastric mucosa vulnerable to mucosal injury.

83.   Twenty patients taking NSAIDs had a histologically normal gastric antral mucosa.

84.   Therefore, agents capable of reducing hypergastrinaemia may be of potential value in preventing the trophic effects of hypergastrinaemia on the gastric mucosa.

85.   Likewise, the carcinogenic action of bile may be related to the duration of exposure of gastric mucosa to biliary carcinogens.

86.   In experimental models of gastric damage, there is evidence that the ability of the gastric mucosa to synthesise prostaglandins plays an important part in mediating adaptive cytoprotection.

87.   Before treatment, H pylori colonisation of the gastric mucosa had been detected by urease test and histology in all patients.

88.   A very strong association of H pylori infection of the gastric mucosa with chronic active type B gastritis and duodenal ulcer has been clearly established by now.

89.   Prolonged use of these medicines is known to harm the gastric mucosa.

90.   The larval stages occur in the gastric glands and can only be seen microscopically following processing of the gastric mucosa.