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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical and experimental dermatology 28 (2003), S. 0 
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford UK : Blackwell Science Ltd.
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To examine whether proton pump inhibitors modify the production of oxygen-derived free radicals and related cytokines in the human gastric mucosa infected with H. pylori.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Thirty-four H. pylori-positive peptic ulcer patients (23 gastric ulcer, 11 duodenal ulcer) were enrolled. Biopsy tissue samples were obtained endoscopically from the antrum and corpus. Tissue content of neutrophil myeloperoxidase (myeloperoxidase) and IL-8 was measured by ELISA. Mucosal production of oxygen-derived free radical was measured using luminol-dependent chemiluminescence (ChL). A proton pump inhibitor (either lansoprazole 30 mg, omeprazole 20 mg, or rabeprazole 10 mg) was administered daily by mouth to all patients for 8 weeks. Endoscopic examination was then repeated, and biochemical analysis was performed.〈section xml:id="abs1-3"〉〈title type="main"〉Results:Antral myeloperoxidase decreased significantly after proton pump inhibitor treatment (5.23 ± 7.00–2.76 ± 5.11 ng/mg, P 〈 0.02), but corpus myeloperoxidase was unchanged. IL-8 was also modified by proton pump inhibitors and these changes were parallel to those of myeloperoxidase. Corpus ChL was significantly increased from 88.5 ± 69.8–159 ± 172 counts/10 s/mg after proton pump inhibitor treatment, whereas antrum ChL was not altered. H. pylori infection rate was decreased in the antrum as well as the corpus.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions:Proton pump inhibitor treatment stimulated oxygen-derived free radical production in the corpus mucosa.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Forty-six H. pylori-infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme-linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks.〈section xml:id="abs1-4"〉〈title type="main"〉Results:In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase 〉 corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase 〉 antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Jejunal endoscopy and histopathological study of biopsied specimens were performed to clarify states of jejunal mucosa and the mechanism of enteric protein loss in six patients with protein-losing enteropathy, including four patients with intestinal lymphangiectasia, one patient with constrictive pericarditis associated with dilated lymphatics of the intestine, and one patient with Budd-Chiari syndrome. Three cardinal endoscopic findings, scattered white spots, white villi, and chyle-like substances covering the mucosa, were demonstrated in protein-losing enteropathy. Scattered white spots indicated markedly dilated lymphatics in the stroma of the villi. White villi seemed to be due to fats including chylomicrons or fat droplets in the absorptive cells, interepithelial spaces, and/or stroma, even though the biopsies were obtained in the fasting state. Therefore, white villi suggest impaired transport of fats from intestinal epithelial cells to intestinal lymphatics. These three cardinal findings are thought to be characteristic for protein-losing enteropathy secondary to lymphatic disorders.
    Type of Medium: Electronic Resource
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