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  • 1985-1989  (2)
  • 1975-1979  (4)
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  • 1
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] It has been shown that tissues such as spleen10, heart and kidney11, tumour cells12 and platelets13 incorporate radiolabelied arachidonic acid into phospholipids and release labelled PGs. It is known that macrophage phospholipids contain a high proportion of this fatty acid14. We have found that ...
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 265 (1977), S. 170-173 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] During a search for potential non-steroidal anti-inflammatory drugs, one was found to possess a high degree of biological activity, yet it was inactive asan inhibitor in the routine PG synthetase assay4. In rat foot oedema, this compound, 2-aminomethyl-4-t-butyl-6-iodophenol (MK-447), exhibited ...
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 27 (1989), S. 451-454 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tumor necrosis factor (rTNF) has previously been shown to induce PMN chemotaxis, stimulate PMN adhesion to vascular endothelium and stimulate hydrogen peroxide secretion from PMNs adhered to biological surfaces. We investigated the activity of both rTNF α and rTNF β on adherent and suspension cultures of human PMNs. rTNF α selectively stimulated the release of the specific granule in a dose dependent manner. Exocytosis of the specific granule was measured with an enzyme-immunoassay for lactoferrin and a radioassay for vitamin B12-binding protein. Adherent PMNs released up to 60% of the total lactoferrin content of the cells with no increase in myeloperoxidase (MPO) secretion when stimulated with 0.1–10NM rTNF α. The PMNs in suspension cultures also selectively released the specific granule, although total release was reduced suggesting that adherence of PMNs increased their ability to respond to physiological stimuli. When PMNs in suspension cultures or adherent cells were stimulated with rTNF α, no LTB4 production was detectable, yet the cells retained the ability to synthesize LTB4 when stimulated with calcium ionophore A23187. Neither rTNF α or rTNF β stimulated the release of the azurophilic granule, measured by the secretion of MPO and neutrophil elastase activity. These results suggest that a function of rTNF α and rTNF β on PMNs is the release of the contents within the specific granule.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gastric bleeding caused by cyclooxygenase inhibitors has been assessed by a novel method. Rats are adapted to a strict light-dark cycle with limited access to food to reduce thestress associated with starvation. Such animals are then labeled with51Cr-red blood cells from donor animals and dosed with the compound under evaluation. After 24 hr. animals are sacrificed and the amount of blood that has accumulated in the lumen of the cecum is quantitated. The potency of cyclooxygenase inhibitors in this assay to cause gastric bleeding is as follows: indomethacin〉piroxicam〉naproxen〉ibuprofen〉diflunisal which is similar to their antiinflammatory potency in the rat. In addition, the protective activity of PGE2 on indomethacin-induced gastric bleeding is clearly shown by this method.
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  • 5
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Evidence that macrophages secrete products that contribute to the central role played by these cells in chronic inflammation continues to accumulate. These products include hydrolytic enzymes active at either acid or neutral pH, prostaglandins, several components of the complement system, factors affecting the responses of T and B lymphocytes to mitogens, factor(s) causing increased proliferation and collagen synthesis by fibroblasts, pyrogen, and interferon. There is little information available concerning the effect of inflammatory stimuli on the secretion of these products. In the case of two types of macrophage secretory products, namely lysosomal acid hydrolases and prostaglandins, there is a marked dependence of their release on the nature of the stimuli presented to the cells. Zymosan or antigen-antibody complexes, which show potent inflammatory activity, cause the selective release of acid hydrolases from macrophages in a dose- and time-dependent fashion. These stimuli also cause the release of [3H]arachidonic acid from phospholipids, with resultant synthesis and secretion of prostaglandins. On the other hand, latex particles, which have minimal inflammatory activity in vivo, fail to cause selective release of lysosomal enzymes from macrophages and do not cause prostaglandin biosynthesis and secretion. The major products of arachidonic acid oxygenation produced by macrophages appear to be PGE2 and 6-keto PGF1α, the stable metabolite of PGI2.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 2 (1977), S. 285-294 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The causal role assigned to the E and F prostaglandins in inflammatory processes, implied by the antiinflammatory action of prostaglandin synthetase inhibitors, is not consistent with the findings reported here that a compound (MK-447) capable of increasing levels of these prostaglandins is antiinflammatory in classical animal models of acute inflammation. That both MK-447 and prostaglandin synthetase inhibitors depress the enzymatic formation of PGG2 from arachidonic acid suggests that this endoperoxide plays a pivotal role in acute inflammation. However, in view of the intermediate nature of PGG2, it seems likely that such a pivotal role for this substance is a function of its ability to be converted to other inflammatory mediators. Possible candidates for a causal role are thromboxane A2 (TXA2) prostacyclin (PGI2), both of which derive from PGG2. However, direct evidence is presented to show that an oxygen equivalent released in the enzymatic conversion of PGG2 to PGH2 is a prime factor in inflammation.
    Type of Medium: Electronic Resource
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