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G. Delvaux

Bio: G. Delvaux is an academic researcher. The author has contributed to research in topics: Antrum & Duodenum. The author has an hindex of 1, co-authored 1 publications receiving 20 citations.

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TL;DR: Observations indicate that inhibition of cell renewal by stress is not the mechanism by which stress erosions develop in the digestive mucosa.
Abstract: Wistar rats were stressed by immobilization in a cold environment during either 2 or 12 h. The animals were killed 1 h after intraperitoneal injection of 3H-thymidine and autoradiography was used. The proliferative parameters were estimated in the mucosa of the stomach after the 2-hour stress period. After the 12-hour stress period, labeling and mitotic indices were measured in the gastric mucosa as well as in the antrum, duodenum, ileum, colon and epidermis. The stress period of 2 h did not induce significant changes of the proliferative parameters in the mucosa of the stomach whereas cell proliferation was significantly inhibited in all examined tissues, including the skin, after the 12-hour stress period. Gastric hemorrhagic lesions were observed only in the oxyntic part of the stomach and occurred as early as 2 h after stress despite there was no change in the proliferative parameters at this time. The lesions became more obvious after the 12-hour stress period. Our observations indicate that inhibition of cell renewal by stress is not the mechanism by which stress erosions develop in the digestive mucosa.

20 citations


Cited by
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TL;DR: An increasing emphasis on central nervous system mechanisms in peripheral disease, especially gastrointestinal disease is noted and many CNS-active agents have been tested for their effects on gastric and duodenal lesion formation and gastric secretion, including antidepressants, antipsychotics, anxiolytics, noradrenergic, serotonergic, dopaminergic, and peptidergic compounds.

286 citations

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TL;DR: Modulation of stress-induced mucosal mast cell activation may help in the management of certain intestinal conditions involving epithelial pathophysiology.
Abstract: We examined the impact of chronic stress on rat growth rate and intestinal epithelial physiology and the role of mast cells in these responses. Mast cell-deficient (Ws/Ws) rats and +/+ littermate c...

209 citations

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TL;DR: The presence of salivary glands attenuates the stress ulcerogenesis probably by releasing epidermal growth factor which acts, in part, by enhancing ornithine decarboxylase activity, mucosal growth, and prostaglandin and glutathione formation.

134 citations

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TL;DR: With increasing attention being paid to mucosal growth and repair as components of mucosaldefense, the emphasis of drug therapy of acute or chronic gastroduodenal lesions is likely to move toward strengthening mucosal defense rather than the inhibition of aggressive factors.

64 citations

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TL;DR: Treatment with ghrelin increases the healing rate of duodenal ulcers and this effect is related, at least in part, to improvement of duODenal mucosal blood flow, mucosal cell proliferation and antioxidant defense, as well as being related to reduction in mucosal oxidative stress and inflammatory response.
Abstract: Background Previous studies have shown that administration of ghrelin exhibits protective and therapeutic effects in the gut. The aim of the present investigation was to examine the influence of ghrelin administration on the course of cysteamine-induced duodenal ulcers, as well as effects on mucosal production of oxygen free radicals and duodenal antioxidant defense.

43 citations