Objective To study the effects and clinical significance of plasma thromboxane B2(TXB2), platelet alpha granule membrance protein-140(GMP-140), 6-Keto-PGF1?(6-K-PGF1?), endothelins(ET), tissue type plasminogen activator(tPA) and plaminogen activator inhibitor-1(PAI-1) in patients with cerebral arteriosclerisis and cerebral thrombosis. Methods Plasma TXB2 ,GMP-140,6-K-PGFla and ET levels were determined by ra-dioimmuno-assay. Plasma tPA and PA1 were determined by the chromogenic peptide substrate method in controls and in patients with cerebral arteriosclerisis and cerebral thrombosis. Results The levels of plasma TXB2 and GMP-140 were significantly higher in patients with cerebral arteriosclerisis and cerebral thrombosis than in the control group(P0.05) .The levels of tPA and tPA/PAI were significantly lower in patients with cerebral arteriosclerisis and cerebral thrombosis than in controls. Although the PAI level increased in patients with cerebral arteriosclerisis and cerebral thrombosis,no difference was found in statistics. Conclusions Activation of platelets, injury of endothelial cell and decreased activity of fibrinolysis in patients with cerebrovascular disease may be involved in the development of these diseases. Appropriate treatment should be adopted on the above abnormality.

We have studied mainly the distribution of this ~3H-labelled schistosomicidal drug in the livers and brains of the albino mice. In livers the ~3H-labelled substances were localized in greater quantity in the liver cell trabecula than in the sinusoids, and were taken up by the Kupffer's cells too. But the most prominent condense localization of the ~3H-labelled substances were in the interlobular bile ducts indicating that the original agent and its metabolites were excreted through the bile ducts system. The nuclei of the liver cells contained a certain amount lof the ~3H-labelled substances, about 7 silver grains in each nucleus with a diameter of about 10.7? seen in 2? thick freezing sections. One of the metabolites of this schistosomicidal drug being a mutagenic agent, the appearance of ~3H-labelled substances in the cell nuclei attracts our great attentions. As for the genesis mechanism of jaundice after administration of this schistosomicidal drug, our opinion is that it might be chiefly the result of drug sensitizied allergy reaction in accordance with a lot of works in the clinics, immunological test, pharmacological principles and our present studies. In the brains, the ~3H-labelled substances distributed much more in the white substances than in the gray substances, with the exception of the substantia nigra which had the same density of number of silver grains as the white substances. With these findingsthe clinical symptoms of the nervous system and their recovery were reviewed.