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Tooth surface-pellicle lipids and their role in the protection of dental enamel against lactic-acid diffusion in man.
Salivary lipids in health and disease.
Helicobacter pylori-induced gastric mucosal TGF-α ectodomain shedding and EGFR transactivation involves Rac1/p38 MAPK-dependent TACE activation
It is demonstrated that up-regulation in H. pylori LPS-elicited Rac1-GTP membrane translocation plays a pivotal role in recruitment of the activated p38 to the membrane for TACE activation through phosphorylation on Thr735.
Isolation and characterization of oligosaccharides from rat colonic mucus glycoprotein.
Structural features of carbohydrate chains in human salivary mucins.
Mechanism of Helcobacter pylori Pathogenesis: Focus on Mucus
These findings indicate that the attachment of H. pylori to the mucosa involves specific structures on the epithelial cell surfaces of the gastric epithelium.
Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol)
- B. Slomiany, C. Kasinathan, A. Slomiany
- Biology, MedicineThe American journal of gastroenterology
- 1 October 1989
Evidence is presented that De-Nol is capable of preventing degradation of mucosal lipids by C. pylori lipases and, hence, helps to preserve the mucosal integrity.
Involvement of constitutive nitric oxide synthase in ghrelin-induced cytosolic phospholipase A2 activation in gastric mucosal cell protection against ethanol cytotoxicity
It is demonstrated that ghrelin protection of gastric mucosa against ethanol cytotoxicity involves cNOS-derived NO induction of cPLA2 activation for the increase in PGE2 synthesis, which apparently includes the c PLA2 phosphorylation followed by S-nitrosylation.
Modulation of gastric mucosal calcium channel activity by sucralfate.
The results indicate that sucralfate has the ability to protect the cellular integrity from calcium imbalance and was inhibited by sucralFate, which also interfered with the binding of EGF to calcium channel protein.
Role of mucus in gastric mucosal protection.
The authors' studies provided strong argument that a bacterial factor, namely infection by Helicobacter pylori through the action of its protease and lipase enzymes also is highly detrimental to the integrity of gastric mucus, and agents capable of interfering with the pathogenic activity of this bacteria are becoming the drugs of choice in peptic ulcer therapy.