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1

The relationship between H. pylori virulence genotypes and gastric diseases

100%
Liu Y. E., Gong Y. H., Sun L. P., Xu Q., Yuan Y.
Polish Journal of Microbiology
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2012
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tom 61
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nr 2
There have been no reports on the relationship between virulence genes and gastric diseases based on the same bacterial colonization density. Our results indicated that Helicobacter pylori virulence genes were more relevant than colonization density as a pathogenic mechanism of gastric diseases, which helps elucidate the pathogenic mechanisms of bacteria and aids in the development of improved strategies for the treatment of gastric disease.
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Role of mucus in gastric mucosal protection

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 2
Even though there is no general agreement as to the mechanism of gastric mucosal protection, the consensus is that the initial brunt of luminal insults falls on the mucus layer which constitutes the only identifiable physical barrier between the gastric lumen and the mucosal surface. The continuous renewal and resilient nature of this layer efficiently counters peptic erosion of the gel, assures its viscoelastic and permselective properties, and provides a milieu for containment of the diffusing luminal acid by mucosal bicarbonate. Disturbances in this delicate balance lead to the impairment of the protective function of mucus resulting in gastric disease. Indeed, the weakening of gastric mucosal defense is intimately associated with the diminished viscoelastic qualities of mucus, decrease in hydrogen ion retardation capacity, and the extensive proteolysis of its mucin component. Although until recently the disintegration of the mucus coat was attributed exclusively to the enhanced activity of intragastric pepsin, our 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. Hence, agents capable of interfering with the pathogenic activity of this bacteria are becoming the drugs of choice in peptic ulcer therapy.
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Effect of ebrotidine on gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide

84%
Slomiany B. L., Piotrowski J., Slomiany A.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 3
4

Effect of Helicobacter sp. infection on the number of antral gastric endocrine cells in swine

84%
Sapierzynski R., Fabisiak M., Kizerwetter-Swida M., Cywinska A.
Polish Journal of Veterinary Sciences
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2007
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tom 10
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nr 2
The aim of the present study was to evaluate the effect of Candidatus Helicobacter suis (CHS) and other Helicobacter sp. different from Candidatus Helicobacter suis (non-Candidatus Helicobacter suis, non-CHS) infection on the number of endocrine G and D cells and G/D cells ratio in antral gastric mucosa in swine. Twenty nine stomachs were obtained from clinical healthy pigs about 6 months old and weighing approximately 100-120 kg after slaughter at abattoir located in central Poland. From each stomach samples of the antral gastric mucosa were taken for histopathology, and PCR examination for presence of Helicobacter genus and Candidatus Helicobacter suis. Samples for histopathology and immunohistochemistry were fixed in 10% buffered formalin. To reveal the expression of gastrin- and somatostatin-producing cells specific antibodies were used. Selected endocrine cells were counted in the midzone of pyloric glands, the results were expressed as a mean of the number of immunoreactive cells in one microscopic field, and as the ratio of gastrin to somatostatin cells (G/D). It can be concluded that some species of swine Helicobacter can alter the number of endocrine cells in gastric antral mucosa. Some of these alterations, for example increase the number of G cells, decrease of the D cells and especially increase of ratio G to D cells can be responsible for development of gastroesophageal ulcers in swine.
5

Antrum and corpus gastric permeability in healthy mice and mice infected with Helicobacter felis

84%
Matysiak T., Hashimoto K., Heyman M., Desjeux J. F., Megraud F.
Journal of Physiology and Pharmacology. Supplement
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1997
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tom 48
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nr 1
6
Content available remote

Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells

67%
Jang S. H., Lim J. W., Kim H.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 7
7
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Up-regulation of endothelin-1 in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide: effect of omeprazole and sucralfate

67%
Slomiany B. L., Piotrowski J., Slomiany A.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 2
8
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Lipopolysaccharide a virulence factor of Helicobacter pylori: effect of antiulcer agents

67%
Piotrowski J.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 1
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Susceptibility of Helicobacter pylori to antimicrobial agents : effect of ebrotidine and ranitidine

59%
Piotrowski J., Piotrowski E., Slomiany A., Slomiany B. L.
Journal of Physiology and Pharmacology
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1995
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tom 46
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nr 4
10

Rozpoznawanie i leczenie zaburzeń motoryki przewodu pokarmowego

34%
Jergens A. E.
Weterynaria po Dyplomie
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2020
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tom 21
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nr 6
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