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  • Key words:β-adrenoceptor agonist — Mast cells — Tryptase — TNF-α— Protein tyrosine phosphorylation  (1)
  • Key words Amyloidosis  (1)
  • Mast cell  (1)
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  • 1
    ISSN: 1420-908X
    Keywords: Key words:β-adrenoceptor agonist — Mast cells — Tryptase — TNF-α— Protein tyrosine phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: This study aimed to evaluate the abil-ity of S1319 (4-hydroxy-7-[1-(1-hydroxy-2-methylamino) ethyl]-1,3-benzothiazol-2(3H)-one acetate), a novel β 2-adrenoceptor selective agonist derived from marine sponge, to inhibit IgE-mediated activation of human cultured mast cells (HCMC) in vitro.¶Materials and Methods: We examined the effect of S1319 (racemate) on tryptase release and tumor necrosis factor- α (TNF-α) production in HCMC generated from human cord blood cells, after cross-linking of high affinity immunoglobulin E receptors (FcεRI), compared with those of the non-selective β-adrenoceptor agonist, isoproterenol (R-isomer), the selective β 2-adrenoceptor agonist, salbutamol (racemate), and the selective and long-acting β 2-adrenoceptor agonist, formoterol (racemate). We also evaluated the effect of S1319 on the intracellular cAMP level, inositol phosphate production and protein tyrosine phosphorylation in HCMC.¶Results: S1319 and β-adrenoceptor agonists inhibited the IgE-mediated release of tryptase. Approximate IC50 values of S1319, formoterol, isoproterenol and albuterol for the inhibition of tryptase release were 0.51 ± 0.12, 0.15 ± 0.1, 0.80 ± 0.09, and 28 ± 32.4 nM, respectively. S1319 and β-adrenoceptor agonists also inhibited TNF-α production by HCMC in a concentration-dependent manner. Approximate IC50 values of S1319, formoterol and isoproterenol for the inhibition of TNF-α production were 0.19 ± 0.03, 0.28 ± 0.02 and 0.32 ± 0.03 nM, respectively. S1319 caused a concentration-dependent increase in total cell cyclic AMP levels in HCMC. On the other hand, S1319 inhibited the accumulation of inositol 1,4,5-triphosphate and IgE-mediated protein tyrosine phosphorylation of 42-kDa protein, p42 mitogen activated protein (MAP) kinase (ERK-2).¶Conclusion: These results indicate that S1319 and β-adrenoceptor agonists are potent inhibitors of the IgE-mediated release of mediators from HCMC.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 328 (1993), S. 59-62 
    ISSN: 0014-5793
    Keywords: Histamine release ; IP3 ; Mast cell ; PI-PLC ; Pedicellarial toxin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2307
    Keywords: Key words Amyloidosis ; ATTR Ser50Ile ; Autopsy ; Familial amyloidotic polyneuropathy ; Transthyretin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We report an autopsy case of a pedigree of familial amyloidotic polyneuropathy (FAP) with a mutation of isoleucine-50 transthyretin (ATTR Ser50Ile). A 47-year-old man started developing severe diarrhea and weight loss at age 41 years, followed by urinary incontinence, autonomic-nervous-system abnormalities and serious heart failure; the diagnosis of FAP (ATTR Ser50Ile) was made on the basis of genetic, histochemical and immunohistochemical analysis. Six years after the initial symptoms, he died of septic shock. Autopsy revealed suppurative peritonitis, perforation of the sigmoid colon and marked systemic amyloid deposition. The total amount of amyloid deposited in the heart was greatly increased and was much lower in the thyroid gland and kidneys compared with amyloid deposits in ordinary FAP (ATTR Val30Met). Amyloid deposition in peripheral vessel walls was prominent, particularly in lymphatics and veins. His elder sister, 54 years old, started to develop orthostatic hypotension at age 49 years, followed by dysesthesia, diarrhea and severe congestive heart failure. Endomyocardial biopsy revealed severe TTR–amyloid deposition; ultrastructural examination demonstrated that amyloid fibrils were deposited disproportionately and extended radially around microvessels. These characteristic patterns of systemic amyloid deposition and distinct clinical manifestations, especially in the cardiovascular system, are considered to be a characteristic feature of ATTR Ser50Ile amyloidosis.
    Type of Medium: Electronic Resource
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