The structure of aqueous solutions of 1:1 salts (KCl, NaCl, KF, and CsI) near a hydrophobic surface is analysed using the angle-dependent integral equation theory. Water molecules are taken to be hard spheres imbedded with multipolar moments including terms up to octupole order, and hard spherical ions are immersed in this model water. The many-body interactions associated with molecular polarizability are treated at the self-consistent mean field level. The effects of cationic and anionic sizes and salt concentration in the bulk are discussed in detail. As the salt concentration increases, the layer of water molecules next to the surface becomes denser but its orientational order remains almost unchanged. The concentration of each ion at the surface can be drastically different from that in the bulk. As a striking example, at sufficiently low salt concentrations, the concentration of I − is about 500 times higher than that of F − at the surface.
Extensive clinical studies of Helicobacter pylori have shown this bacterium to be an important causative factor of peptic ulcer, particularly in its recurrence. Therefore, numerous therapeutic trials for the eradication of H. pylori have been reported. A recent trend in curative therapy has been so-called triple therapy, using a proton pump inhibitor and two different antimicrobials. 1 Sucralfate, which is a widely used cytoprotective agent for the gastric mucosa, is reported to inhibit several of the activities of H. pylori and to enhance the anti-H. pylori activity of antimicrobial agents. 2±11 Therefore, several studies of sucralfate-based eradication therapy have been reported recently. 12±18 However, the ef®cacy and safety of sucralfate-based therapy are still controversial. 19±20 The present study was designed to evaluate the ef®cacy and safety of sucralfate in combination with amoxycillin and clarithromycin as eradication therapy for H. pylori, in comparison with lansoprazole-based triple therapy.
PATIENTS AND METHODS
PatientsThis study was designed as a prospective, randomized, multicentre study, and was carried out in accordance SUMMARY Background: Sucralfate has an inhibitory action against Helicobacter pylori and enhances the anti-H. pylori activity of antimicrobials. Aim: To evaluate the ef®cacy and safety of sucralfatebased eradication therapy for H. pylori infection, compared with that based on lansoprazole, in a randomized multicentre study. Subjects and methods: The subjects were 150 H. pyloripositive patients. They were randomly assigned to one of two regimens for 2 weeks: sucralfate 1 g t.d.s., amoxycillin 500 mg t.
Background
: Ecabet sodium, a novel non‐systemic anti‐ulcer agent, possesses high affinity to gastric adherent mucus, which plays an important role in the protection of the gastric epithelium against acid and pepsin.
Aim
: To assess the effect of ecabet on pepsin‐induced degradation of the structure of the mucus gel layer.
Methods
: Everted sacs of rat stomach were incubated in HCl solution containing pepsin with or without ecabet. Pepsin‐induced release of the cleaved peptides and hexosamine from the sacs was determined. Changes in the molecular size of glycoproteins in the adherent mucus (using gel filtration methods) and in the morphology of the epithelium (using both light and scanning electron microscopy) were also examined.
Results
: Ecabet reduced the pepsin‐induced release of peptides and hexosamine, depending on its content in the adherent mucus. Pepsin treatment partially lowered the molecular weight of native glycoproteins in the adherent mucus, caused exfoliation of the epithelial cells, and degraded the network‐like ultrastructure of the mucus layer, giving it a lumpy, globular appearance. Ecabet prevented both the pepsin‐induced molecular size shift in mucus glycoproteins, and morphological alteration of the epithelium, including ultrastructural derangement of the mucus gel layer.
Conclusion
: Ecabet protects the polymeric structure of mucus glycoproteins from proteolytic degradation by pepsin, and thus maintains integrity of the gastric mucus gel layer.
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