Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was aimed at assessing whether epidermal growth factor (EGF) and its receptors are present in the gastric mucosa during the healing of gastric ulcers. Immunohistochemical, immunochemical and functional studies were performed in rats after induction of ulcers in the oxyntic mucosa. Controls, which included non-operated and sham-operated animals, displayed only rare cells in the bottom of the oxyntic glands showing EGF-like immunoreactivity. Within one day after ulcer induction, a markedly increased number of chief cells in undamaged mucosa showed intense staining. Concomitantly, there was an increased immunoreactivity for EGF receptors in the mucous neck cells. Maximal immunostaining for both compounds was observed at 3 days after ulcer induction; augmented staining was still demonstrable after 3 weeks. RIA revealed significantly increased EGF concentration in the oxyntic mucosa three days after ulcer induction, and at this stage stimulated gastric acid secretion, measured in a parallel group of chronic fistula rats, indicated significant inhibition. The transient increases in EGF-like and EGF receptor immunoreactivities may stimulate gland cell proliferation. The local release of EGF-like substances may also serve to reduce gastric acidity and thereby promote ulcer healing.
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PMID:Immunoreactivities for epidermal growth factor (EGF) and for EGF receptors in rats with gastric ulcers. 193 26

Human epidermal growth factor (EGF), a small polypeptide (6 kDa) with mitogenic properties, has been implicated in the protection of gastrointestinal mucosal integrity. The efficacy of EGF in the prevention and healing of sclerotherapy-induced esophageal lesions was investigated in 24 minipigs with surgically induced portal hypertension. In addition, the effect of EGF on intragastric acidity and pharmacokinetics was investigated as possible means to explain its protective mechanism of action. The animals underwent three weekly sessions of sclerotherapy with polidocanol 2% and were concomitantly and for an additional three weeks treated with either placebo or EGF administered paravenously in the esophagus and/or subcutaneously. The subcutaneous treatment with EGF significantly (P < 0.05) reduced esophageal stricture and scar formations associated with sclerotherapy. Gastric pH values were significantly (P < 0.01) elevated only in animals receiving subcutaneous injections of EGF. Furthermore, the subcutaneous administration of EGF was associated with unexpected prolonged plasma concentration of the peptide. These results suggest a possible clinical value of EGF as an adjunctive treatment with the sclerotherapy.
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PMID:Systemic treatment with recombinant human epidermal growth factor accelerates healing of sclerotherapy-induced esophageal ulcers and prevents esophageal stricture formations in pigs. 799 95

Most antacids contain magnesium and/or aluminium hydroxide but some include also bicarbonate and calcium carbonate. The net effect of antacid action is the reduction in gastric acidity and in peptic activity but recent studies indicate that aluminium-containing antacids exhibit the cytoprotective activity or enhancement of natural mucosal defense mechanisms. This protective action has been attributed, in part, to the release of endogenous prostaglandins but other mediators such as hexa-aquo-aluminium cation and nitric oxide have also been proposed. Aluminium-containing antacids are known to accelerate the healing of chronic gastroduodenal ulcerations and this has been attributed primarily to their acid neutralizing capacity. Since antacids interact with luminal epidermal growth factor (EGF) which exhibits ulcer healing properties it has been proposed that this peptide is implicated in the healing of gastroduodenal ulcerations by these drugs.
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PMID:New aspects of clinical pharmacology of antacids. 826 Jul 35

The effect of epidermal growth factor (EGF) on alkaline secretion and mucus formation which serve as defenses against mucosal injury was investigated using a perfusion system of the proximal duodenum in rats in situ. In control rats, intravenous or intraduodenal administration of EGF (1 or 10 micrograms/kg/hr) had no effect on mucosal alkaline secretion at high (pH 2.5-3.0) or low (pH 3.0-5.5) luminal acidities. In cysteamine-treated rats (250 mg/kg weight, intramuscular injection), mucosal alkaline secretion by intravenous EGF (10 micrograms/kg/hr) increased significantly only at levels of high luminal acidity, whereas that by intraduodenal EGF (10 micrograms/kg/hr) increased greatly at both high and low luminal acidities. Analysis by a color image processor revealed that cysteamine greatly reduced the PAS-stained mucus in the duodenal mucosa and in Brunner's glands. Intraduodenal administration of EGF significantly increased the PAS-stained mucus in the duodenal mucosa, but not in Brunner's glands. These results indicate that EGF exerts the cytoprotective effect by stimulating alkaline secretion and mucus formation in the duodenal mucosa.
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PMID:Effects of epidermal growth factor on alkaline secretion and mucus formation in rat duodenum exposed to luminal acid. 837 22

The previously accepted role of gastric acid hypersecretion in peptic ulcer disease has been modified by studies showing no correlation between acid output and clinical outcome of ulcer disease, or between ulcer recurrence rate after vagotomy and preoperative acid secretion. At the same time, studies have been unable to demonstrate increased acidity in the duodenal bulb in patients with duodenal ulcer, and consequently more emphasis has been given to the mucosal protecting mechanisms. The existence of an active gastric and duodenal mucosal bicarbonate secretion creates a pH gradient from the luminal acid to near neutrality at the surface of the epithelial cells, thereby acting as an important mucosal defence mechanism. The regulation of bicarbonate secretion is a complex process related to motility and neural activity. Stimulation is by acid, PGE2, NO, VIP, cAMP, and mucosal protective agents. Bicarbonate secretion is inhibited by atropine, muscarinic antagonists, alpha-adrenoceptor agonists, indomethacin, bile acids, tobacco smoking, and probably also by infection by Helicobacter pylori. Apart from mucus and bicarbonate, the mucosal defence is supported by a hydrophobic epithelial lining, rapid cell removal and repair regulated by epidermal growth factor. Sufficient mucosal blood flow, including a normal acid/base balance, is important for subepithelial protection. In today's model of ulcer pathogenesis, gastric acid and H. pylori work in concert as aggressive factors, with the open question being: why does only a fraction of the infected population develop an ulcer?
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PMID:Peptic ulcer pathophysiology: acid, bicarbonate, and mucosal function. 872 73

Among the pathogenetic phenomena of Parkinson's disease, the character of the selective degeneration of nigrostriatal system with severe gliosis is not fully understood. Here, we have shown that dopaminergic neurons may be exclusively sensitive to elevated acidity elicited after the addition of glial mitogenic factors such as epidermal growth factor and basic fibroblast growth factor or after the direct treatment with hydrochloric acid. The acid sensitivity was specific to dopaminergic neurons. The neurons other than dopaminergic neurons in culture from the ventral mesencephalon were not sensitive to acidity and the neurons from several brain areas were the same as above, except for the hippocampal neurons which had slight acid vulnerability. Choline acetyltransferase assay studies demonstrated that the cholinergic neuronal population in the septum and corpus striatum had no acid sensitivity. The vulnerability of dopaminergic neurons either elicited by glial mitogenic factor or derived from the direct acid exposure was inhibited by the addition of brain-derived neurotrophic factor (BDNF), but not by neurotrophin-3 or nerve growth factor. These findings suggest that dopaminergic neurons have selective acid vulnerability on which BDNF has a pronounced protective effect.
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PMID:Selective acid vulnerability of dopaminergic neurons and its recovery by brain-derived neurotrophic factor. 878 12

This study was performed to define the biologically active growth modulators in human gastric juice. Mitogenic activity was evaluated by the incorporation of [3H]thymidine into 3T3 fibroblasts. A negative correlation was observed between pH and mitogenic activity in gastric juice (r = -0.45, P < 0.01). The concentrations of epidermal growth factor (EGF), transforming growth factor-alpha and -beta 1 (TGF-alpha and -beta 1), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF) in gastric juice did not explain these changes in mitogenic activity. Gel filtration identified growth-stimulating activity due to small molecule mitogens (less than 13 kDa), and growth inhibitory activity only in neutral samples due to a macromolecular substance (larger than 240 kDa) susceptible to trypsin digestion and heat and acid treatments. We conclude that acidity-dependent changes in mitogenic activity observed in this study are due to appearance of acid-unstable, high-molecular-weight, growth-inhibitory substance.
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PMID:Mitogenic properties of human gastric juice. 928 44

Rab7, a member of the Rab family of small G proteins, has been shown to regulate late endocytic traffic and lysosome biogenesis, but the exact roles and the mode of actions of Rab7 are still undetermined. Accumulating evidence suggests that each Rab protein has multiple target proteins and works together with them to coordinate the individual step of vesicle traffic. Rabring7 (Rab7-interacting ring finger protein) is a Rab7 target protein that has been isolated using a CytoTrap system. This protein shows no homology with RILP, which has been reported as another Rab7 target protein. Rabring7 is recruited efficiently to late endosome/lysosome by the GTP-bound form of Rab7. Exogenous expression of Rabring7 not only affects epidermal growth factor degradation but also induces the perinuclear aggregation of lysosomes and the increased acidity in the lysosomes. This chapter describes the procedures for the isolation of Rabring7 with a CytoTrap system, the analysis of the Rab7-Rabring7 interactions, and the properties of Rabring7.
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PMID:Rabring7: a target protein for rab7 small g protein. 1647 30