30 research outputs found
Effect of prostaglandin on human platelet
Based on the previous report concerning the structure-activity relationship in which inhibiting and stimulating agents for platelet aggregation were able to bind both receptors of human platelet for aggregation and its inhibition, the present experiment was performed to study on the effect of prostaglandins (PGE1, PGI2 and PGD2) on the aggregation and its inhibition of human platelets.
Assuming that PGE1 and PGD2 have conformations for inhibition of platelet aggregation and those for aggregation, changes of cyclic AMP (cAMP) content and of ultrastructure of platelets in the presence of 2', 5'-dideoxyadenosine (DDA, an inhibitor of adenyl cyclase), PGE1 and PGD2 were investigated. When treated with physiological saline, PGE1, PGD2 or DDA alone, aggregation of the platelets was not observed. The platelets were solitarily dispersed. Though most of the platelets showed smooth surface, some platelets showed slight, small elevation and conical depression on the surface. A few platelets possessed one or two short projection at the margin, but no long projection was observed.
The platelets treated with PGE1 or PGD2 in combination with DDA showed markedly elongated projections which is one of the ultrastructural characteristics of activated form of platelets, and were finally aggregated. The most platelets gathered in groups were discoid in form and others showed irregular forms. They had one or sometimes several long pseudopods. It was noted that the pseudopods protruded from the marginal region of the platelets, and were contact with pseudopods of other platelets. The long pseudopods supposed to be the elongation of the spiny and short projections described above. At first, small protrusions appeared on the entire surface of the platelets. They showed a clear tendency to adhere to each other, formed small and larger aggregates, and resulted in more and more firm aggregation. This feature may represent the first stage of transformation for aggregation of platelets. The round protrusion became large in size and increase in number.
The present study pointed out the importance of the concomitant presence of receptors for the aggregation and its inhibition in the platelet plasma membrane
Effect of amino acid mixtures on nasal allergic responses induced by toluene diisocyanate in mice
We studied the effect of various amino acid mixtures on nasal allergy induced by the intranasal application of toluene diisocyanate (TDI) in mice. In Experiment 1 (Exp. 1), mice were fed a 25% casein, soy protein isolate (SPI), egg white protein (EW) or gluten diet. In Experiment 2 (Exp. 2), mice were fed a 25% amino acid mixture diets patterned after casein (AA-casein), SPI (AA-SPI), EW protein (AA-EW) or gluten (AA-gluten). In Experiment 3 (Exp. 3) we modified the glutamine/glutamic acid (Gln/Glu) concentrations in the amino acid mixtures. Mice were fed a 25% AA-SPI, low Gln/Glu AA-SPI (LG-AA-SPI), AA-EW or high Gln/Glu AA-EW (HG-AA-EW) diet. At the 5th week, mice were divided into sensitized (sen-) and non-sensitized (ns-) groups. The mice in sensitized groups were treated with two courses of intranasal application of toluene diisocyanate (TDI) in ethyl acetate for 5 consecutive days, separated by 9 days rest. The non-sensitized groups of mice were treated with a vehicle. Nine days after the second sensitization, all mice were provoked by TDI. Nasal responses and serum IgE concentration were studied. The findings of Exp. 1 showed that the sen-EW group exhibited a lower body weight gain, higher nasal symptom score and higher IgE concentration than the other sensitized groups. The findings of Exp. 2 showed that the sen-EW group had a lower body weight gain, higher nasal symptom score and higher IgE concentration than the other sensitized groups. In Exp. 3, the AA-EW group showed a higher total nasal score and IgE concentration than the HG-AA-EW group, however, the findings of LG-AA-SPI and AA-SPI were similar. These findings demonstrated that amino acid mixtures affect nasal allergy induced by the intranasal application of TDI in mice