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Featured researches published by Zv Healey.


Gastroenterology | 1997

How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology.

John Calam; Anita Gibbons; Zv Healey; Pw Bliss; Naila Arebi

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.


Peptides | 1998

EFFECT OF PACAP-27 ON 14C-AMINOPYRINE ACCUMULATION IN ISOLATED RABBIT PARIETAL CELLS

Zv Healey; Pw Bliss; Jason Edwards; Naila Arebi; Ian L.P. Beales; John Calam

Pituitary adenylate cyclase-activating polypeptide (PACAP) is present in gastric mucosa, but its direct effect on parietal cells is unknown. We examined this using 14C-aminopyrine uptake in elutriated rabbit cells. PACAP-27 had no effect on basal cells but significantly increased the response to histamine (10(-4) M) at 10(-9) M and to carbachol (10(-4) M) in the presence of ranitidine (10(-4) M) at 10(-7) M and 10(-8) M. PACAP (6-38), an antagonist of PACAP, inhibited the effect of PACAP-27 on carbachol-stimulated cells. Vasoactive intestinal peptide had no significant effect. In conclusion, PACAP-27 has a direct additive effect on stimulated rabbit parietal cells in vitro.


Gastroenterology | 2002

Nitric oxide regulates the release of somatostatin from cultured gastric rabbit primary D-cells

Naila Arebi; Zv Healey; Pw Bliss; M. A. Ghatei; Susan Van Noorden; Raymond J. Playford; John Calam


Gastroenterology | 2000

Epidermal growth factor protects the gastric mucosa by enhancing somatostatin secretion from D-cells

Naila Arebi; Zv Healey; Pw Bliss; M. A. Ghatei; John Calam


Gastroenterology 116(4 PART | 1999

Effect of hyperosmolar sodium chloride on primary rabbit parietal cell acid secretory potential in vitro

Zv Healey; Naila Arebi; John Calam


Clinical Science | 1999

Nitric Oxide Releases Somatostatin from Gastric D-Cells in Rabbit Primary Cell Culture

Naila Arebi; Zv Healey; Pw Bliss; M. A. Ghatei; John Calam


Gastroenterology | 1998

Gastrin release mediated by H2 receptors

Pw Bliss; Zv Healey; Naila Arebi; John Calam


Gastroenterology | 1998

The sialic acid binding lectin from Maackia amurensis inhibits 14C-aminopyrine accumulation by rabbit parietal cells: Implications for Helicobacter pylori adhesins

Zv Healey; Pw Bliss; Naila Arebi; John Calam


Gastroenterology | 1998

Broad bean and concanavalin a lectins inhibit 14C-aminopyrine accumulation by rabbit parietal cells in primary culture

Zv Healey; Mark Jordinson; Pw Bliss; Naila Arebi; John Calam


Gastroenterology | 1998

Soya bean lectin and broad bean lectin stimulate gastrin release from rabbit G cells in primary culture

Pw Bliss; Mark Jordinson; Zv Healey; Naila Arebi; John Calam

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John Calam

Imperial College London

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Pw Bliss

Imperial College London

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Naila Arebi

Imperial College London

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M. A. Ghatei

Imperial College London

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Naila Arebi

Imperial College London

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Raymond J. Playford

Queen Mary University of London

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