1. Pure ethanol does not stimulate gastrin release in humans.

2. To overcome this problem we have measured gastrin mediated acid secretion after the intravenous infusion of gastrin releasing peptide.

3. Future studies evaluating mechanisms of gastrin release have to take into account the H pylori state.

4. The role of the increased serum gastrin concentration induced by H pylori in the pathogenesis of duodenal ulcer disease is also unknown.

5. Similarly, basal serum gastrin concentrations do not alter with ageing in healthy men.

6. Carbachol, gastrin, and histamine all bind to specific receptors on parietal cell plasma membranes.

7. Our finding that fasting serum gastrin consists mainly of G34 is consistent with previous reports.

8. For gastric acid secretion, basal serum gastrin was considered in addition to these three variables.

9. They found that patients with the highest serum gastrin concentrations did not necessarily have the highest enterochromaffin like cell counts.

10. The potential autocrine grown effects of gastrin in colorectal cancer have previously been studied using cell lines.

11. The serum gastrin concentration was determined by radioimmunoassay using antibody R98.

12. Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing perse.

13. There was no relationship between the serum gastrin concentration and type of renal replacement treatment.

14. This was also true when gastrin and intrinsic factor were incubated together with their respective antibodies.

15. The plasma gastrin concentrations increased from group to group as expected from the dose given.

16. The exaggerated acid response to gastrin can be explained by the increased parietal cell mass present in duodenal ulcer patients.

17. Serum gastrin concentrations did not correlate well with changes in the endocrine cell density.

18. Gastrin levels may also be elevated by pernicious anemia. duodenal ulcers, and after a meal.

19. Integrated meal stimulated serum gastrin outputs were determined by calculating the area under the serum concentration time curve.

20. H pylori has variable effects on serum gastrin concentrations and gastric acid secretion.

21. Helicobacter pylori increases plasma gastrin concentrations by 50% to 100% and values fall to normal after the organism has been eradicated.

22. The finding of enhanced fasting gastrin concentrations in H pylori positive subjects and in duodenal ulcer disease can not easily be explained.

23. Subjects with atrophy had significantly higher serum gastrin concentrations than all other subjects and higher than old subjects without atrophy.

24. There have been conflicting reports concerning the form of gastrin that is increased in H pylori infection.

25. Most investigators have observed that H pylori infection causes a greater percentage increase in the postprandial gastrin than fasting gastrin.

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26. Further characterisation of the non-ethanolic component of beer and wine that stimulates acid and gastrin secretion needs to be carried out.

27. We therefore also plotted individual dose-response curves of log plasma gastrin against the basal-subtracted acid output.

28. In another study by Ryberg etal the enterochromaffin like cell labelling index was shown to increase linearly with the plasma gastrin concentration.

29. Our finding also confirms previous reports that postprandial serum gastrin consists of approximately equivalent concentrations of G17 and G34.

30. It seems possible that this material originates from rare mucosal endocrine cells expressing the gastrin gene.

31. Gastrin is the designation given to a family of protein hormones produced by the mucosal cells of the gastric antrum.

32. Serum gastrin concentration was measured by radioimmunoassay with antibody R98 as previously described.

33. Recent work has focused on the gastrin acid secretion feedback loop and identified a number of potential pathogenetic pathways.

34. Plasma gastrin concentration was measured by radioimmunoassay with antibody G179 provided by Professor Bloom.

35. Obviously, this differentiation can readily be made by measurement of serum gastrin.

36. It is this dual defect that causes their considerable sixfold increase in gastrin mediated acid secretion.

37. We measured circulating gastrin to determine the concentrations of gastrin required to produce half maximal acid secretion.

38. Hence, many of these patients may actually have supramaximal gastrin concentrations.

39. At this time the basal and meal stimulated gastrin concentrations were reassessed as described above.

40. This correlation argues for the possibility of synthesis of platelet activating factor precursors in cells sensitive to gastrin stimulation.

41. Discussion Our current results confirm that treatment which both heals duodenal ulcers and eradicates H pylori significantly decreases basal plasma gastrin concentrations.

42. Kothary etal have reported that terminally extended forms of gastrin in conjunction with G14 are more prevalent in duodenal ulcer patients.

43. Antral gastrin and somatostatin cell densities and fasting serum gastrin concentrations were similar in the two groups of patients with Zollinger-Ellison sydrome.

44. Gastritis with atrophy and the consequent loss of acid mediated inhibition of gastrin release contributes most to this increase.

45. To ensure accuracy, gastrin measurements were performed in the same assay batch.

46. The plasma gastrin concentrations in the various groups increased in the same order of magnitude as expected from the gastrin dose given.

47. After eradication of H pylori in the duodenal ulcer patients both their basal acid output and basal gastrin fell by 50%.

48. In man and other species, there is accumulating evidence that gastrin stimulates acid secretion by releasing histamine.

49. Gastrin is a gut hormone produced by G cells located in the gastric antrum.

50. Antisera R526 was raised in rabbit to synthetic human gastrin fragment 1-17 of G34, coupled to chicken egg albumen using glutaraldehyde.

51. Increased basal serum gastrin is related to atrophy and to infection with H pylori.

52. Despite this reduction in plasma gastrin, no consistent changes in rates of acid secretion have been documented after eradication treatment.

53. Bombesin, Gastrin Releasing Peptide (GRP), Rabbit anti.

54. Methods: The gastrin levels in the arterial and venous blood of the cancer area and its cancer tissues, paracancer mucosas, and normal mucosas by radioimmunoassay in 26 patients with gastric cancer .

55. Curcuma Longa probably include the excitant or antagonist of gastrin receptor.

56. Subsequent to DPG - BII and PPSG serum gastrin, which increased after HSV(/gastrin.html), decreased.

57. All types of vagotomy cause an increase of basal and postprandial serum gastrin levels.

58. Zollinger-Ellison syndrome is a disorder where increased levels of the hormone gastrin are produced, causing the stomach to produce excess hydrochloric acid.

59. The effects of electrical damage of the nucleus raphe magnuson gastric acid output and serum gastrin level in anesthetized rats were observed.

60. To explore the relation between personality, mental status, serum gastrin and functional dyspepsia and its subgroups.

61. The gene is called GRPR for gastrin - releasing peptide receptor.

62. The gene is called the GRPR for ( gastrin ) releasing ( peptide ) receptor.

63. Objective To study the change of the serum gastrin(GAS)and plasma motilin(MTL)levels as well as the gastric motility in gastric cancer patients after subtotal gastrectomy.

64. Gastrin and cholecystokinin and secretin act on the same target organs.

65. The results suggested that in ADU patients the increase of BAO, which is relating to the increase of antral gastrin content, may contribute to the activity of DU.

66. Method The serum levels of gastrin, glucogan and somatostatin were detected by radioimmunoassay.

67. The result of immuno-electron cytochemistry showed the number of positive reaction cells of gastrin increased significantly.

68. The results showed that Rhizoma Curcuma Longa probably include the excitant or antagonist of gastrin receptor.

69. Objective To study the secretion phase about plasma gastrin ( GAS ), motilin ( MOT ) and somatostatin ( SS ) in diabetic gastroparesis ( DGP ).

70. The biochemical era in the study of gastrin was initiated.

71. Studies have proved that gastrin plays key roles in the development and progression of gastroenteric tumor.

72. Elevated serum levels of GI peptides such as vasoactive intestinal polypeptide (VIP) and gastrin may be present with secretory diarrhea.

73. The gastrin and the glucagon cells were not found in the alimentary canal.

74. Omeprazole stimulates liver regeneration after reduced - size liver transplantation and this regeneration may be mediated by gastrin.

75. Conclusions: There are receptors of gastrin, somatostatin and muscarine on the ECL cell surfaces.

76. The gene is called GRPR for dextrin ( gastrin ) releasing peptide receptor.

77. The level of serum gastrin, plasma motilin, plasma endotoxin, and the ratio of lactulose to mannitol in urine(L/M ratio) were measured on the 1st, 3rd, 7th(), and 10th day after burn injury.

78. The serous levels of gastrin, glucogan and somatostatin were detected by radioimmunosive assay.

79. Peptone solution perfused into the antral pouch was used as a potent gastrin releaser and the acid output of the stomach was taken to indicate the release of gastrin from the antral mucosa.

80. Serotonin, somatostatin and gastrin releasing peptide positive cells were not found in fetal endometrium.

81. The body weight, body temperature, mean retention time of chyme in digestive tract, gastric emptying velocity, gastrin and motilin levels, and visceral index of mice.

82. The level of serum gastrin (LSG) and tongue signs of 113 patients which were randomly collected with the double blind method were investigated.

83. The genge is called GRPR for gastrine releasing gastrin - releasing peptide receptor.

84. The genge is called GRPR for gastrin gastrin - releasing peptide receptor.

85. Chen XH, Li DG. Serum gastrin level changes in patients with thalamic hemorrhage complicated with GI tract bleeding.

86. The expression of gastrin had no relationship with dukes stages, PCNA expression and p 53 protein expression.

87. Objective To explore the effects of optional cesarean section on the level of plasma motilin and serum gastrin in umbilical blood and their relationship with gastroenteric symptoms of neonates.

88. Signal transduction pathway mediates motilin - and gastrin - induced contraction of antral smooth muscle cells was investigated in rats.