Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...