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  • Articles: DFG German National Licenses  (2)
  • Electronic Resource  (2)
  • 1990-1994  (1)
  • 1985-1989  (1)
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  • Articles: DFG German National Licenses  (2)
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  • Electronic Resource  (2)
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Year
  • 1
    Electronic Resource
    Electronic Resource
    The role of a Ca2+/calmodulin dependent plasma membrane Ca2+ channel during Concanavalin A activation of MC9 mast cells (1987)
    Springer
    Inflammation research 22 (1987), S. 16-23 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of Con A on free cytoplasmic calcium concentrations in the cloned murine mast cell, MC9, have been measured using the fluorescent calcium indicator quin 2. Con A causes a rapid, small yet sustained rise in free cytosolic calcium (up to 245 nM) followed closely by increased45calcium uptake and more slowly by histamine release. The increases in45calcium uptake and histamine release require extracellular calcium. However, the Ca2+ influx blockers, nifedipine and verapamil inhibit these responses only at concentrations significantly higher than those used in smooth muscle to oppose potential-dependent events, and diltiazem is inactive. These observations suggest that, in these mast cells, other types of channels control Ca2+ entry. In contrast, the intracellular Ca2+ blocker, TMB-8, inhibits both the Con A-induced histamine release and the Ca2+ changes. The calmodulin antagonists calmidazolium, trifluoperazine and W-7 are also highly effective inhibitors of both the Ca2+ changes and histamine release in direct proportion to their potency against calmodulin-dependent phosphodiesterase, implicating calmodulin in the regulation of stimulus-secretion in MC9 cells. These data imply that histamine release follows increases in intracellular Ca2+ concentration. Free intracellular Ca2+ results from rapid release from internal stores and is followed by a slower but more sustained influx of extracellular Ca2+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01968811
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Naphthalenes as inhibitors of myeloperoxidase: Direct and indirect mechanisms of inhibition (1990)
    Springer
    Inflammation research 29 (1990), S. 266-276 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Control of myeloperoxidase (MPO) may be an important consideration in disorders where excessive PMN elastase activity is a significant factor. There are, however, two mechanisms for the apparent regulation of MPO: i) inhibit the enzyme directly, and ii) prevent the ensuing HOCl induced oxidation by using a surrogate reducing agent. Appropriate methodology has been devised to distinguish true MPO inhibitors. With the exception of NaN3, many MPO inhibitors fall into the latter category and do not actually regulate the enzyme. Several potent organic inhibitors have been discovered, which, because of their structural selectivity, appear to associate specifically with a binding site on the enzyme, rather than attaching indiscriminately to a hydrophobic domain. By controlling the enzyme, these compounds protect α-1-PI from MPO induced damage, and could serve better than antioxidants to define the role of MPO in elastase induced injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01966457
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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