Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: TAKEUCHI
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Tytuł oryginału: Gastric hyperemic response induced bay acid back-diffusion in rat stomachs following barrier disruption - relation to vanilloid type-1 receptors.
Autorzy: Tashima Kimihito, Nakashima Masato, Kagawa Shigeru, Kato Shinichi, Takeuchi Koji
Źródło: Med. Sci. Monitor 2002: 8 (5) s.BR157-BR163, il., bibliogr. 20 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • farmacja
  • gastroenterologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Acid back-diffusion activates capsaicin-sensitive sensory neurons (CSN), leading to gastric hyperemic response. We examined the role of vanilloid type-1 receptor (VR1) in gastric hyperemic and ulcerogenic responses in rat stomach following exposure to taurocholate (TC). Under urethane anesthesia, a rat stomach was mounted on an ex-vivo chamber, perfused with 50 mM HCl, and changes in PD, gastric mucosal blood flow (GMBF), and luminal acid loss were measured before and after exposure to 20 mM TC for 30 min, in presence of omeprazole. Capsazepine was co-applied with TC for 30 min to the stomach, while ruthenium red was given i.v. 10 min before TC treatment. TC caused a marked PD reduction, followed by an increase of acid loss and GMBF, resultin in minimal damage in the mucosa. Chemical ablation of CSN attenuated the GMBF response to TC without affecting PD reduction and acid loss, and resulted in severe lesions, while none of these responses induced by TC was significantly affected by either capsazepine or ruthenium red. Intragastric capsaicin increased GMBF, and this response was attenuated by both capsazepine and ruthenium red as well as sensory deafferentation. Both acid back-diffusion and capsaicin increase GMBF mediated by CSN, yet their modes of action differ in terms of capsazepine- or ruthenium red-sensitvity. Although the luminal H+ plays a modulator role for the physiological response mediated by CSN in the stomach, it is unlikely that the action results from the interaction of H+ with the capsazepine- or ruthenium red-sensitive site of VR1.

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    Tytuł oryginału: Type I interferons as immunoregulatory molecules; implications for therapy in experimental autoimmune uveoretinitis.
    Autorzy: Mizuguchi Junichiro, Takeuchi Masaru, Usui Masahiko
    Źródło: Arch. Immunol. Ther. Exp. 2002: 50 (4) s.243-254, bibliogr. 125 poz.
    Sygnatura GBL: 304,223

    Hasła klasyfikacyjne GBL:
  • immunologia
  • farmacja
  • okulistyka

    Typ dokumentu:
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • zwierzęta
  • szczury

    Streszczenie angielskie: Clinical trials have shown that type I interferon (IFN)-ŕ/á have some beneficial effects on organ-specific autoimmune diseases, such as Behcet's diseases and multiple sclerosis, although the precise mechanisms remain largely unresolved. T helper cells 1(Th1)-mediated autoimmune responses are involved in the initiation and/or progression of human uveitis, such as Behcet's disease. The animal model of experimental autoimmune uveoretinitis (EAU), characterized by a monophasic clinical course, has contributed to the understanding of the pathogenesis of human uveitis. Th1 producing IFN-ç induce EAU development, while Th2 producing IL-4/IL-10 prevent the disease. However, depending on the cytokine milieu, the pro-inflammatory cytokine IFN-ç may attenuate the autoimmune responses and anti-inflammatory cytokine IL-4 exacerbates it. Chemokines also play a crucial role in EAU development, which might be resolved by Th2-mediated immune responses. The administration of IFN-ŕ/á prevents EAU development, accompanied by a diminished production of IFN-ç/IL-10. Interestingly, however, IFN-ŕ/á also have some beneficial effects on patients with Th2-like phenotype in addition to Th1-like phenotype. Thus, the immuno-modulatory action of IFN-ŕ/á may be dependent on the context of cytokine combinant and/or their concentrations.

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