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  • 1985-1989  (4)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 25 (1988), S. 57-59 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Treatment of rabbit chondrocytes with natural or recombinant human IL 1 results in a dramatic dose-dependent increase in intracellular phospholipase A2 (PLA2) activity and subsequent secretion of this enzyme into the intracellular millieu. PLA2 activity is detectable as early as 1 hr after IL 1 stimulation and is maximal by 24 hr. In the present study, we have characterized more fully the relationship between PLA2 activation and arachidonate metabolism in these cells. IL 1 treatment of chondrocytes which had been prelabeled with [14C] arachidonic acid resulted in an enhanced release of free arachidonic acid identified by thin-layer chromatography. Moreover, the arachidonic acid liberated was subsequently metabolized exclusively to PGE2; no significant increases in the production of 6-keto PGF1α, LTB4, LTC4, 12-HETE or 15-HETE were observed following IL 1 stimulation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract When activated in autologous mixed leukocyte reactions (auto-MLR)in vitro, T cells from normal individuals produce a suppressor factor(s) which inhibits the Epstein-Barr virus (EBV)-induced proliferation of normal B cells. In contrast, T cells from patients with rheumatoid arthritis (RA) are deficient in their ability to generate this suppressor factor in auto-MLR. Addition of tilomisole (Wy-18,251; 3-(p-chlorophenyl)thiazolo[3,2-a]benzimidazole-2-acetic acid) to the auto-MLR (0.1–100 μg/ml) did not alter the production of suppressor activity by normal T cells, but 100 μg/ml tilomisole restored to normal the defective factor production by RA T cells. Indomethacin (1 μg/ml) but not levamisole (0.1–100 μg/ml) had a similar effect, which suggests that the action of tilomisole in this system is due to its ability to inhibit prostaglandin biosynthesis. Nonetheless, the ability of tilomisole to down-regulate B cell function may contribute to the compound's antiarthritic activity.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 78 (1989), S. 179-184 
    ISSN: 1432-1106
    Keywords: Neurotransmitter ; High pressure nervous syndrome ; Synaptosome ; Monoamine ; Pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary High pressure exposure produces neurological changes which manifest as tremors, EEG changes and convulsions. Since previous studies have implicated the involvement of the monoaminergic system in these symptoms, it was of interest to study monoamine release at high pressure. Synaptosomes isolated from guinea pig brain were used to follow monoamine efflux at 68 ATA. The major observation was a decrease in the initial calcium dependent release of all three monoamines in response to K+ induced depolarization. This response is similar to that previously observed for GABA, glycine and glutamate. This generalized pressure induced depression of initial transmitter release suggests a mechanism common to the release process for both excitatory and inhibitory neurotransmission.
    Type of Medium: Electronic Resource
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