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Sökning: L773:0065 4299

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1.
  • Andersson, Rolf G, et al. (författare)
  • Studies of the mechanism of desensitization of anti-IgE-mediated histamine release from human basophils
  • 1989
  • Ingår i: Agents and actions. - 0065-4299. ; 27:1-2, s. 25-28
  • Tidskriftsartikel (refereegranskat)abstract
    • Human basophils became hyporesponsive to anti-IgE when exposed to this agent in the absence of Ca2+ for more than 10 min. The desensitization process proceeded in parallel to the releasing-process. The mechanism of desensitization seems to involve a very early step in the release-reaction, since the response to phospholipase A2 and diolein, agents involved in the release-reaction, was not affected by the desensitization.
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2.
  • Carlin, G, et al. (författare)
  • Effect of anti-inflammatory drugs on xanthine oxidase and xanthine oxidase induced depolymerization of hyaluronic acid.
  • 1985
  • Ingår i: Agents and actions. - 0065-4299. ; 16:5, s. 377-84
  • Tidskriftsartikel (refereegranskat)abstract
    • The inhibitory effect of various anti-inflammatory drugs on the xanthine oxidase derived depolymerization of hyaluronic acid was studied. The depolymerization was assayed by repeated viscosity measurements. By using a low xanthine oxidase activity, the decrease in viscosity with time followed first order reaction kinetics and was therefore suitable for kinetic analysis. The xanthine oxidase activity was monitored by assay of O2-consumption with a Clark-electrode and by assay of urate production. We present evidence that salicylic, acetylsalicylic, gentisic and azodisalicylic acid and sulfasalazine inhibit the production of oxygen-derived free radicals by xanthine oxidase. We found that sulfapyridine, 5-aminosalicylic acid, allopurinol, mannitol, glucuronic acid and N-acetylglucosamine in addition to the earlier studied drugs, paracetamol, ibuprofen, benoxaprofen and gentisic acid exert their effect via scavenging of free radicals. These drugs had very little effect on the enzyme activity.
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3.
  • Nilsson, B O, et al. (författare)
  • Release of polyamines in cultures of rat parotid and liver cells
  • 1993
  • Ingår i: Agents and Actions. - 0065-4299. ; 38:1 suppl., s. 44-47
  • Tidskriftsartikel (refereegranskat)abstract
    • Rat parotid gland and liver cells were cultured for 6 and 24 h. The cells as well as their growth medium were analyzed on their content of the polyamines putrescine, spermidine and spermine. In control medium the content of polyamines was very low but already after 6 h substantial amounts of all three polyamines under study had been released into the medium from parotid as well as from liver cells. The release was much more pronounced from parotid compared to liver cells. Putrescine was accumulated in parotid cells as well as in the medium indicating that a new synthesis of this amine occurred in these cells.
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4.
  • Thomsen, P, et al. (författare)
  • Inhibitory effect of honey bee venom on immune complex mediated leukocyte migration into rabbit knee-joints
  • 1984
  • Ingår i: Agents and Actions. - 0065-4299. ; 14:5-6, s. 662-666
  • Tidskriftsartikel (refereegranskat)abstract
    • The anti-inflammatory effect of purified honey bee venom (HBV) was studied using a recently described animal model in which preformed immune complexes were injected into rabbit knee-joints. As little as a single injection of 1.2 micrograms HBV/kg body weight subcutaneously significantly reduced the immune complex induced joint inflammation as measured by reduction in leukocyte counts in the joint fluid. This decrease was obvious 3 and 6 but not 9 hours after induction of the inflammation. There was no significant effect on leukocyte random migration, chemotactic responsiveness or phagocytosis, indicating that HBV did not interfere with normal phagocyte motility and ingestion. The modifying effects by HBV on the inflammatory response to immune complexes in vivo is most likely due to interference with other components of the inflammatory response.
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5.
  • Toll, Johan B, et al. (författare)
  • Effects of mepacrine and p-bromophenacyl bromide on anti-IgE and phospholipase A2-induced histamine release from human basophils
  • 1986
  • Ingår i: Agents and actions. - 0065-4299. ; 18:5-6, s. 518-523
  • Tidskriftsartikel (refereegranskat)abstract
    • Exposure of human basophils to purified phospholipase A2 caused a release of histamine, the process could be divided in one Ca2+-independent and one Ca2+-dependent stage. Low concentrations of mepacrine and p-bromophenacyl bromide (BPB) inhibited both phospholipase A2- and anti-IgE-induced histamine release. Mepacrine was more potent than BPB when the two-stage-method was used. The inhibition of mepacrine was most effective when the drug was added in the second Ca2+-dependent stage. The effect of mepacrine in the whole reaction of the anti-IgE-induced histamine release was biphasic and mepacrine was less effective than in the inhibition of the separated stages. The effect of BPB on the whole reaction was rather similar to mepacrine, although it was not biphasic. The results presented in this work confirm a previous hypothesis suggesting that activation of phospholipase A2 is an important step in the IgE-mediated histamine release process. The results also suggest that inhibition of histamine release due to inhibition of phospholipase A2 might be of therapeutical value as the system can be inhibited at very low drug concentrations.
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