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Factors influencing the restitution of the duodenal and colonic mucosa after damage

100%

Riegler M., Feil W., Wenzl E., Schiessel R.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 1

Rapid epithelial restitution is an important protective mechanism which enables the gastrointestinal mucosa to reestablish epithelial integrity following superficial injury within hours. In this study we examined the influence of an acidic luminal pH, removal of the necrotic layer, nutrient bicarbonate, calcium and sodium desoxycholate (Na-DOC) on restitution in the rabbit duodenum in vitro and the role of Na-DOC and calcium for rapid restitution of the human colon in vitro. Transmucosal potential difference (PD), short-circuit current (lsc) were measured and resistance against passive ion flux (R) was calculated. Electrophysiological changes paralleled morphological injury but did not necessarily reflect restitution in all experiments. The extent of mucosal injury was assessed by computerized real-time morphometry. 5 hrs after luminal exposure to 10 mH HCl for 10 min residual damage (RD) was 14% in the duodenum. Luminal pH of 3.0 (RD of 30%), removal of necrotic layer at acidic luminal pH (RD of 66%), absence of bicarbonate from the serosal solution (RD of 35 % at neutral luminal pH; RD of 96% at acidic luminal pH) and removal of calcium from the serosal solution (RD of 58 %) impaired restitution in the duodenum. Continuous postinjury luminal Na-DOC exposure did not influence restitution in the duodenum (RD of 19%). 5 hrs after luminal exposure to 0.5 mM Na-DOC for 10 min RD was 26% in the human colon. Continuous postinjury luminal Na-DOC exposure (RD of 51 %) and removal of calcium from the nutrient solution (RD of 65 %) impaired restitution in the human colon. Thus we conclude that restitution of the rabbit duodenum in vitro requires a necrotic layer and bicarbonate flux to withstand acidic luminal pH, while restitution is not Effected by Na-DOC. In the human colon Na-DOC inhibits restitution. Both the duodenum and colon require calcium for rapid restitution.

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Analysis of immediate ex vivo release of nitric oxide from human colonic mucosa in gastrointestinally mediated allergy, inflammatory bowel disease and controls

100%

Raithel M., Hagel A. F., Zopf Y., Bijlsma P. B., De Rossi T. M., Gabriel S., Weidenhiller M., Kressel J., Hahn E. G., Konturek P. C.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 4

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The influence of anti-TNF therapy on CD31 and VEGF expression in colonic mucosa of Crohn’s disease patients in relation to mucosal healing

100%

Eder P., Lykowska-Szuber L., Iwanik K., Krela-Kazmierczak I., Stawczyk-Eder K., Majewski P., Linke K., Kay E. W., Wozniak A.

Folia Histochemica et Cytobiologica

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2016

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tom 54

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nr 2

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DNA damage in human colonic mucosa cells induced by bleomycin and the protective action of vitamin E

100%

Wozniak K., Arabski M., Malecka-Panas E., Drzewoski J., Blasiak J.

Cellular and Molecular Biology Letters

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2004

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tom 09

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nr 1

Using the alkaline comet assay, we showed that bleomycin at 0.1-5 μg/ml induced DNA strand breaks and/or alkali-labile sites, measurable as the comet tail moment, in human colonic mucosa cells. This DNA damage was completely repaired during a 120-minute post-treatment incubation of the cells. Post-treatment of the bleomycin-damaged DNA with 3-methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing alkylated bases, gave rise to a significant increase in the extent of DNA damage, indicating that the drug could induce alkylative bases in DNA. We did not observe any change in the comet tail moment in the presence of catalase. Vitamin E ((+)-α-tocopherol) decreased DNA damage induced by bleomycin. The results obtained suggest that hydrogen peroxide might not be involved in the formation of DNA lesions induced by bleomycin in the colonic mucosa cells, and that vitamin E may exert protective effects on these cells.

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Ornithine decarboxylase in large bowel mucosa: regulation by gastrin, secretin and EGF

100%

Johnson L. R., Wang P., Haddox K.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 1

Rats were fasted 48 h and then injected once with either saline, pentagastrin, EGF, secretin or combinations of secretin and pentagastrin or EGF. Another group of rats was fasted and refed. Animals were killed 4 h later and ODC assayed in mucosa of the cecum, proximal colon, and distal colon. EGF significantly increased ODC activity in all 3 tissues. Secretin had no effect by itself on ODC or ODC stimulated by EGF. Pentagastrin significantly increased ODC of the cecum, and secretin completely inhibited the effect of pentagastrin. Refeeding fasted rats significantly induced activity in all three tissues. Immunocytochemistry using a highly specific polyclonal ODC antibody showed that ODC was confined to the crypt cells of the proximal colon. Antibody dilution techniques demonstrated that gastrin, EGF and refeeding increased the level of enzyme in these cells. Refeeding in addition caused the appearance of enzyme in surface epithelial cells. These results showed that colonic mucosal ODC is present in proliferative cells and is regulated by the same peptides known to regulate growth in this tissue. Colonic mucosal ODC also responds the same way as it does in the oxyntic gland and small bowel mucosa.

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Expression and release of leptin and proinflammatory cytokines in patients with ulcerative colitis and infectious diarrhea

80%

Biesiada G., Czepiel J., Ptak-Belowska A., Targosz A., Krzysiek-Maczka G., Strzalka M., Konturek S. J., Brzozowski T., Mach T.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 5

Ograniczanie wyników

Factors influencing the restitution of the duodenal and colonic mucosa after damage

Analysis of immediate ex vivo release of nitric oxide from human colonic mucosa in gastrointestinally mediated allergy, inflammatory bowel disease and controls

The influence of anti-TNF therapy on CD31 and VEGF expression in colonic mucosa of Crohn’s disease patients in relation to mucosal healing

DNA damage in human colonic mucosa cells induced by bleomycin and the protective action of vitamin E

Ornithine decarboxylase in large bowel mucosa: regulation by gastrin, secretin and EGF

Expression and release of leptin and proinflammatory cytokines in patients with ulcerative colitis and infectious diarrhea