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Biomedical subjects

M Nilius

Publications and source records attributed to M Nilius.

22 records · Page 2Linked to original sources

[Polymorphism in Helicobacter pylori--a key function in recurrence of infection?].

Despite the fact that Helicobacter (H.) pylori is ubiquitous throughout the world, little is known at present about the source of infection and mode of transmission. Person-to-person transmission may be of importance. The fact that Helicobacter pylori can revert to a coccoid form stimulated speculation about its role in transmission and as a possible cause of reinfection in duodenal ulcer disease. Various antibacterial agents (bismuth subcitrate 32 mg/l bismuth subsalicylate 64 mg/l, amoxicillin 0.05 mg/l, ampicillin 2 mg/l, erythromycin 4 mg/l, glycochenodeoxycholic acid 423 mg/l, ursodeoxycholic acid 540 mg/l) inhibit the growth of H. pylori and stimulate the formation of coccoid structures. Ultrastructural and biochemical results show that the coccoid form meets the necessary criteria for survival. Thus, to be successful, treatment must aim not only at eliminating the vegetative form, but also at preventing the development of the coccoid form.

Anti-Bacterial Agents↗

In vitro inhibition of Helicobacter pylori urease: biochemical and ultrastructural analysis.

Inhibition of H. pylori urease was studied by means of electron-microscopy and electrophoretic methods using different urease inhibitors, such as acetohydroxamic-acid (AHA), L-ascorbic acid (AsA), copper ions, a combination of L-ascorbic acid with copper ions and UV light. AHA in two different concentrations and AsA at a concentration of 0.1 mg ml-1 showed incomplete inhibition of H. pylori urease activity in our electrophoretic experiments. Only membrane-bound activity was inhibited with AHA but not the activity localized within the cytoplasma as demonstrated by electron-microscopy. AsA at a concentration of 0.5 mg ml-1 and the combination of copper ions (1 microgram ml-1) with AsA completely inhibited the urease activity as demonstrated by electron-microscopy and electrophoretic experiments. Cu2+ ions in high concentrations (100 micrograms ml-1) and UV light exposure for more than 4 h induced a complete disintegration of H. pylori. Electrophoresis showed no active protein after UV light exposure of 2 h. Different urease inhibitors tested in this study showed dose-dependent inhibitory effects on H. pylori urease in vitro.

Ascorbic Acid↗