Search PubMed⌕ Search

Biomedical subjects

C Ra

Publications and source records attributed to C Ra.

114 records · Page 7Linked to original sources
PubMed1988

Thromboxane A2 production in allergen-induced immediate and late asthmatic responses. Its possible role in inducing the late response.

To determine whether thromboxane A2 (TXA2) participates in allergen-induced asthmatic responses, we measured plasma TXB2 levels during allergen-induced immediate and late asthmatic responses (IAR and LAR) in atopic asthmatics. We also examined the effect of a TXA2 synthetase inhibitor, OKY-046, on the responses. Plasma TXB2 levels increased in both IAR and LAR, being 2.2 times higher in LAR than in IAR. Plasma TXB2 levels in LAR reached the peak 4 hours after allergen challenge when FEV1 had just begun to decrease in LAR. OKY-046 inhibited both IAR and LAR with decreased plasma TXB2 levels. We conclude that TXA2 is produced in allergen-induced asthmatic responses and participates in the responses, especially in inducing LAR.

Adult↗
PubMed1986

Comparative evaluation of the effect of pharmacological agents on endocytosis and coendocytosis of IgE by rat basophilic leukaemia cells.

The aggregation of IgE bound to rat basophilic leukaemia (RBL) cells leads to the exocytosis of mediators, the endocytosis of the antigen-aggregated mouse IgE anti-DNP, as well as the coendocytosis of some unaggregated monomeric rat IgE (IR162) and/or unbound receptors. We describe here the relative effect on endocytosis and coendocytosis of various pharmacological agents that block or enhance exocytosis. We have previously shown that, unlike exocytosis, endocytosis by RBL and normal rat mast cells was independent of extracellular calcium. We show here that the presence of calcium chelators or antagonists also had no effect on endocytosis of cross-linked IgE. However, coendocytosis of non-cross-linked IgE was partially inhibited by the elimination of extracellular calcium and the addition of calcium chelators such as EDTA or EGTA-Mg2+. Moreover, the addition of calcium antagonists such as Ni2+ and Co2+ (5 mM) to an incubation mixture containing Ca2+ (1 mM) resulted in the complete inhibition of coendocytosis without affecting endocytosis. Other inhibitors of exocytosis such as sodium azide (10-2M), quercetin (10-4M) and dibutyryl cyclic AMP (10-2 M) blocked coendocytosis completely but had no effect on endocytosis. Sodium azide (10 mM) in combination with 2-deoxyglucose (10 mM) effectively inhibited (90%) endocytosis. Cytochalasin B (10-4 M), which was shown to enhance serotonin release, had no effect on the extent of endocytosis or coendocytosis observed 20 min after the initiation of aggregation. Thus, in RBL cells, endocytosis, coendocytosis and exocytosis exhibit distinguishable sensitivities to some pharmacological drugs.

Animals↗
PubMed1985

Arachidonic acid metabolism of human granulocytes from asthmatic patients.

Granulocytes from asthmatic patients produced more LTC4 than did normal granulocytes on calcium ionophore stimulation. When granulocytes were stimulated, the rate of increase of AA metabolite participating in bronchospasm was significantly higher in asthmatic granulocyte than in normals; however, the rates of increase in bronchodilating metabolite showed no difference. After stimulation, the total amounts of AA metabolites in asthmatic granulocytes and normal granulocytes showed no difference; however, the ratio between bronchodilating AA metabolites and bronchoconstricting AA metabolites was higher in asthmatic granulocytes.

Arachidonic Acid↗