Antral G-cell and D-cell numbers in Helicobacter pylori infection: effect of H. pylori eradication.

[1]  S. Asnaes,et al.  Variation in distribution of antral gastrin cells. , 2009, Acta pathologica et microbiologica Scandinavica. Section A, Pathology.

[2]  J. Polak,et al.  Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease , 1992, The Lancet.

[3]  D. Graham,et al.  Factors influencing the eradication of Helicobacter pylori with triple therapy. , 1992, Gastroenterology.

[4]  I. Lemaire.  Bombesin-related peptides modulate interleukin-1 production by alveolar macrophages , 1991, Neuropeptides.

[5]  D. Graham,et al.  Effect of triple therapy (antibiotics plus bismuth) on duodenal ulcer healing. A randomized controlled trial. , 1991, Annals of Internal Medicine.

[6]  K. McColl,et al.  Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. , 1991, Gut.

[7]  W. Karnes,et al.  Elevation of meal-stimulated gastrin release in subjects with Helicobacter pylori infection: reversal by low intragastric pH. , 1991, Reviews of infectious diseases.

[8]  R. Pounder,et al.  Eradication of Helicobacter pylori abolishes 24‐hour hypergastrinaemia: a prospective study in healthy subjects , 1991, Alimentary pharmacology & therapeutics.

[9]  D. Graham,et al.  Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients , 1991 .

[10]  D. Graham,et al.  Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea ingestion. , 1991, Gastroenterology.

[11]  D. Graham.  I. Helicobacter pylori: Its epidemiology and its role in duodenal ulcer disease , 1991, Journal of gastroenterology and hepatology.

[12]  M. Dixon.  IV. Helicobacter pylori and peptic ulceration: Histopathological aspects , 1991, Journal of gastroenterology and hepatology.

[13]  K. McColl,et al.  Plasma gastrin, daytime intragastric pH, and nocturnal acid output before and at 1 and 7 months after eradication of Helicobacter pylori in duodenal ulcer subjects. , 1991, Scandinavian journal of gastroenterology.

[14]  J. Holton,et al.  Serum pepsinogen I and gastrin concentrations in children positive for Helicobacter pylori. , 1990, Journal of clinical pathology.

[15]  D. Graham,et al.  Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. , 1990, The American journal of gastroenterology.

[16]  F. Marotta,et al.  Relationship between gastrin cell number, serum, antral mucosa and luminal gastrin concentration and gastric acidity in antral atrophic gastritis. , 1990, Gut.

[17]  E. A. Sankey,et al.  Immunostaining of antral gastrin cells is quantitatively increased in Helicobacter pylori gastritis , 1990, Histopathology.

[18]  R. Playford,et al.  Antral Helicobacter pylori, hypergastrinaemia, and duodenal ulcers: effect of eradicating the organism. , 1989, BMJ.

[19]  G. Fullarton,et al.  LOWERED GASTRIN AND GASTRIC ACIDITY AFTER ERADICATION OF CAMPYLOBACTER PYLORI IN DUODENAL ULCER , 1989, The Lancet.

[20]  R. Playford,et al.  CAMPYLOBACTER PYLORI AND DUODENAL ULCERS: THE GASTRIN LINK , 1989, The Lancet.

[21]  A. Opekun,et al.  CAMPYLOBACTER PYLORI DETECTED NONINVASIVELY BY THE 13C-UREA BREATH TEST , 1987, The Lancet.

[22]  T. Adrian,et al.  Gastroduodenal mucosal hormone content in duodenal ulcer disease. , 1985, Hepato-gastroenterology.

[23]  P. Sipponen,et al.  Morphology and dynamics of the gastric mucosa in duodenal ulcer patients and their first-degree relatives. , 1983, Hepato-gastroenterology.

[24]  H. Shimazu,et al.  G-cell populations in resected stomachs from gastric and duodenal ulcer patients , 1980 .

[25]  J. H. Baron,et al.  G cell population of the gastric antrum, plasma gastrin, and gastric acid secretion in patients with and without duodenal ulcer. , 1978, Gut.

[26]  J. Mary,et al.  Gastrin cell distribution in normal human stomachs and in patients with Zollinger-Ellison syndrome. , 1978, Gastroenterology.

[27]  F. Keuppens,et al.  Estimation of the antral and duodenal gastrin cell population removed by gastrectomy from patients with peptic ulcer. , 1978, Surgery, gynecology & obstetrics.

[28]  W. Creutzfeldt,et al.  Mucosal gastrin concentration, molecular forms of gastrin, number and ultrastructure of G-cells in patients with duodenal ulcer. , 1976, Gut.

[29]  R. Herrera-Llerandi.  Letter: Amoeba in stools. , 1975, Lancet.

[30]  J. Piris,et al.  Quantitation of G-cells in fibreoptic biopsy specimens and serum gastrin levels in healthy normal subjects. , 1975, Journal of clinical pathology.

[31]  S. Bloom,et al.  Proceedings: The relationship between gastric emptying rate and plasma enteroglucagon concentration. , 1975, Gut.

[32]  J. Polak,et al.  Proceedings: Endocrine quantitation of clinical gastric biopsies. , 1975, Gut.

[33]  B. Blackwell,et al.  EXPERIENCE WITH 45 RENAL HOMOTRANSPLANTATIONS IN MAN. , 1965, Lancet.

[34]  J. Myren,et al.  Gastric Secretion and Parietal Cells , 1963 .

[35]  Card Wi,et al.  The relationship between the acid output of the stomach following "maximal" histamine stimulation and the parietal cell mass. , 1960 .

[36]  W. Creutzfeldt,et al.  Histopathological classification of nonantral gastric endocrine growths in man. , 1988, Digestion.

[37]  H. Krämling,et al.  Antigen-induced gastrin release: an immunologic mechanism of gastric antral mucosa. , 1987, Advances in experimental medicine and biology.

[38]  P. Brandtzaeg,et al.  Immunohistochemical investigation of gastrin-producing cells (G cells). Estimation of antral density, mucosal distribution, and total mass of G cells in resected stomachs from patients with peptic ulcer disease. , 1978, Scandinavian journal of gastroenterology.

[39]  P. Brandtzaeg,et al.  Quantification of gastrin-producing cells (G cells) and parietal cells in relation to histopathological alterations in resected stomachs from patients with peptic ulcer disease. , 1978, Scandinavian journal of gastroenterology.

[40]  P. Brandtzaeg,et al.  Quantitative studies of gastrin cells (G cells) and parietal cells in relation to gastric acid secretion in patients with peptic ulcer disease. , 1978, Scandinavian journal of gastroenterology.

[41]  F. Baldi,et al.  Antral G cells and mucosal gastrin concentration in normal subjects and in patients with duodenal ulcer. , 1978, Advances in experimental medicine and biology.

[42]  E. Gjone,et al.  Fasting and food-stimulated serum gastrin concentrations in relation to the antral G-cell population. A study in patients with peptic ulcer disease. , 1978, Scandinavian journal of gastroenterology.

[43]  M. Rizzetto,et al.  G-cell counts in antral endoscopic biopsies by immunofluorescence. , 1977, Scandinavian journal of gastroenterology.

[44]  P. Brandtzaeg,et al.  Immunohistochemical investigation of gastrin-producing cells (G cells).The distribution of g cells in resected human stomachs. , 1976, Scandinavian journal of gastroenterology.

[45]  F. Stadil,et al.  Measurement of immunoreactive gastrin in gastric mucosa. , 1975, Scandinavian journal of gastroenterology.

[46]  J. Myren,et al.  Gastric secretion and parietal cells. I. The relationship between the rates of secretion and the intracellular succinic dehydrogenase activity in resected human stomachs. , 1963, Gastroenterologia.