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  • 2000-2004  (3)
  • 2002  (3)
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  • 2000-2004  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background We have recently demonstrated that the transfer of interleukin (IL)-5-producing CD4+ T cell clones into unprimed mice is sufficient for the development of eosinophilic inflammation in the bronchial mucosa upon antigen inhalation.Objective The aim of this study was to elucidate the possible contribution of mast cells in eosinophilic inflammation and bronchial hyper-responsiveness (BHR), and to discriminate between the roles of CD4+ T cells and mast cells.Methods Mast cell-deficient mice (WBB6F1-W/Wv) and their congenic normal littermates (WBB6F1−+/+) were immunized with ovalbumin and challenged by inhalation with the relevant antigen.Results Airway eosinophilia was induced with equivalent intensity in +/+ and W/Wv mice 6, 24, 96 and 216 h after antigen inhalation. In contrast, 48 h after antigen challenge, eosinophilic infiltration into the bronchial mucosa was significantly less pronounced in W/Wv mice than in +/+ mice. Anti-CD4 monoclonal antibody (mAb), anti-IL-5 mAb, and cyclosporin A were administered next, demonstrating that the airway eosinophilia of W/Wv mice induced 48 h after antigen challenge was almost completely inhibited by each of these three treatments, but that of +/+ mice was significantly less susceptible. Bronchial responsiveness to acetylcholine was increased 48 h after antigen challenge and was not significantly different between +/+ and W/Wv mice. Administration of anti-IL-5 mAb completely inhibited the development of BHR in both +/+ and W/Wv mice.Conclusion These results indicate that, in mice, mast cells do have a supplemental role in the development of pulmonary eosinophilia but not BHR. CD4+ T cells totally regulate these responses by producing IL-5.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford UK : Blackwell Science Ltd.
    Journal of fish diseases 25 (2002), S. 0 
    ISSN: 1365-2761
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Pathological changes in cultured tiger puffer, Takifugu rubripes, with emaciation disease in Kyushu, Japan were studied histologically. In most cases, diseased fish were heavily infected with at least one of three myxosporeans (Myxidium fugu, Myxidium sp. and Leptotheca fugu) and two unidentified hyperparasitic microsporeans, attached to, or in, the intestinal epithelium. Myxidium fugu attached to the surface of the epithelium, caused no noticeable effects on the host tissue, irrespective of its infection with the hyperparasite. Myxidium sp., which proliferated in the epithelium, induced severe pathological changes including accumulation of cell debris between the epithelium and lamina propria and resultant detachment of the epithelium. Leptotheca fugu, another histozoic myxosporean, induced degeneration of the epithelium, associated with massive infiltration of macrophages into the epithelium to encapsulate parasites. When L. fugu was infected with its hyperparasitic microsporean, shortened villi were also observed. This is probably because passage of macrophage-parasite aggregates through the basement membrane of the epithelium severely damaged the epithelial structure. It is evident histologically that, unlike epicellular M. fugu, histozoic Myxidium sp. and L. fugu with or without hyperparasitic microsporeans, were highly pathogenic to host fish. This strongly suggests that they are causative agents of the emaciation disease.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aim : To investigate the inhibitory effects on gastric acid secretion of three proton pump inhibitors, omeprazole, lansoprazole and rabeprazole, using a three-way crossover design in healthy Helicobacter pylori-negative,S-mephenytoin 4′-hydroxylase (CYP2C19) homo- and hetero-extensive metabolizers.Methods : Eight healthy Japanese male volunteers were enrolled. After the administration of rabeprazole (10 mg/day), lansoprazole (30 mg/day) or omeprazole (20 mg/day), intragastric pH monitoring was commenced from 24 h before the first proton pump inhibitor dose, and continued for days 1–3 after proton pump inhibitor administration. The pH electrode was used for 48 h and changed just before pH monitoring on day 2.Results : For the administration of 10 mg/day rabeprazole, the mean ratios of the 24-h pH ≥ 3 holding timewere 5.7 ± 1.1%,13.6 ± 2.2%, 35.3 ± 2.7% and 62.8 ± 3.1% for the pre-treatment day and days 1, 2 and 3, respectively. The same ratios for lansoprazole (30 mg/day) were 5.7 ± 0.7%, 7.4 ± 1.5%, 13.6 ± 3.4% and 26.6 ± 4.9%; the same ratios for 20 mg/day omeprazole were 5.9 ± 0.9%, 6.1 ± 1.2%, 11.4 ± 2.8% and 16.4 ± 4.6%. The mean ratio of the 24-h pH ≥ 3 holding time of days 1–3 increased significantly compared to the pre-treatment day (P 〈 0.01) with the administration of rabeprazole and lansoprazole. The magnitude of inhibition of gastric acid secretion after rabeprazole administration was stronger than that after lansoprazole. A significant elevation of the mean ratio of the 24-h pH ≥ 3 holding time was demonstrated on days 2 and 3 with omeprazole (P 〈 0.01).Conclusions : In H. pylori-negative CYP2C19 extensive metabolizers, rabeprazole (10 mg/day) shows a faster onset of rising intragastric pH and a stronger inhibition of gastric acid secretion than do lansoprazole (30 mg/day) or omeprazole (20 mg/day).
    Type of Medium: Electronic Resource
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