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  • Articles: DFG German National Licenses  (3)
  • 1985-1989  (3)
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  • Articles: DFG German National Licenses  (3)
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Years
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 30 (1985), S. 95S 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Agents such as ethanol, aspirin, bile acids, and hypertonic urea and glucose, are capable of breaking the physiological gastric mucosal barrier and may cause ultrastructural injury to the epithelial cells within several minutes of exposure. Ethanol at any pH, and aspirin and bile acids at acid pH, are lipid soluble and diffuse rapidly into surface epithelial cells where a sequence of injury can be documented by electron microscopy. First, the nuclear chromatin becomes clumped and the density of the cytoplasmic ground substance decreases. Second, mitochondria become swollen and the apical cell membrane is distorted. Finally, the apical, cell membrane ruptures and the cell disintegrates. Throughout this sequence, the tight junctions between cells appear morphologically intact. In contrast to lipid soluble agents, hypertonic urea and glucose do not diffuse well into surface epithelial cells. Although these agents also cause rapid changes in transmucosal potential difference and ion fluxes, their ultrastructural effects are quite different. Hypertonic urea and glucose initially cause small blebs within the tight junctions and larger vacuoles within the cytoplasm of surface epithelial cells, while the remainder of the cell structure appears normal. More severe injury is characterized by more vacuolization and eventual disruption of epithelial cells. These changes presumably are secondary to osmotic shifts of fluid and electrolytes. Although the ‘cytoprotective’ effects of prostaglandins have been well described, there is virtually no information at the ultrastructural level concerning the protective effects of prostaglandins with regard to these ulcerogenic agents.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 33 (1988), S. 1064-1069 
    ISSN: 1573-2568
    Keywords: hydrocortisone ; corticosteroids ; epithelial renewal ; epithelial proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to determine whether parenteral administration of steroids affects epithelial renewal in hamster stomach. Male golden hamsters received either hydrocortisone sodium succinate or saline intraperitoneally for three days. In the first experiment, hamsters were sacrificed 1 hr after injection of tritiated thymidine ([3]HTdR) to label proliferating cells. In the second experiment, hamsters were sacrificed hourly after a single [3H]TdR injection up to 48 hr in order to determine cell cycle time by the method of fraction of labeled mitoses. In the third experiment, hamsters were sacrificed 1, 24, and 72 hr after [3H]TdR injection for the study of epithelial migration and cell turnover time. Sections of fundic and antral mucosae were prepared for light autoradiography. Steroid treatment caused no gross or microscopic injury to gastric mucosa, but the number of [3H]TdR-labeled cells as well as the thickness of the proliferative zone were reduced significantly in fundic mucosa, but not in antral mucosa. The study of the fraction labeled mitoses indicated that steroid treatment lengthened the cell cycle time in fundic mucosa, which was due primarily to prolonged G1 and DNA synthesis phases. Furthermore, epithelial migration was significantly slower in fundic mucosa after steroid treatment, which was associated with a prolonged cell turnover time. Thus, parenteral steroids depress the entire process of epithelial renewal in hamster fundic mucosa.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: esophageal cancer ; epithelial proliferation ; carcinogenesis ; N-methyl-N-amylnitrosamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to investigate the histogenesis of experimental tumors in the rat esophagus. Thirty rats received 0.0015% N-methyl-N-amylnitrosamine (MNAN) in the drinking water for 12 weeks. Another 30 rats received tap water. All rats then received tap water until sacrifice. Rats from each group were sacrificed immediately after MNAN administration, four weeks after, and eight weeks after. One hour before sacrifice, [3H]TdR was injected by tail vein to label proliferating cells. The entire esophagus and stomach were removed and processed for light and electron microscopy and autoradiography. The overall frequency of esophageal tumors after MNAN was 83% and did not differ significantly among the three experimental groups. Tumors were primarily papillomas and squamous cell carcinomas and occurred with equal frequency in the upper, middle, and lower thirds of the esophagus. No tumors were found in the squamous-lined forestomach. Electron microscopy revealed abundant tonofilaments, free ribosomes, and mitochondria accompanied by vacuoles. By autoradiography, esophageal epithelial proliferation was markedly stimulated in nontumorous mucosa from all three experimental groups. We conclude that MNAN ingestion for 12 weeks reliably produces papillomas and squamous cell carcinomas throughout the rat esophagus, but not in the squamouslined forestomach, and that MNAN stimulated marked epithelial proliferation which is accompanied by thickening of the epithelium in nontumorus esophageal mucosa.
    Type of Medium: Electronic Resource
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