Yasuharu Nishida

A new rapid and simple assay for factor XIII activity using dansylcadaverine incorporation and gel filtration

A new sensitive, reproducible and simple assay for factor XIII activity was developed, in which fluorescent dansylcadaverine (DC) is incorporated into casein and DC-casein is separated from free DC by gel filtration. A good correlation was found between our method and Lorands. The main advantages of our method are: (1) our assay technique is simple with good reproducibility and takes only a couple of hours; (2) the detectable limit of factor XIII activity is about 1% of normal pool plasma, but, if necessary, can be lowered by increasing the sample amount and lengthening the reaction time.

Substantial expression of glycoproteins IX and V on the platelet surface from a patient with Bernard-Soulier syndrome

Summary. Flow cytometric studies demonstrated that the platelets from a patient with Bernard‐Soulier syndrome expressed substantial amounts of both GPIX and GPV, although in reduced amounts.

Effect of Plasminogen Activator on Platelet Aggregation

The clinical efficacy of thrombolytic therapy with plasminogen activator (PA) may be partly influenced by its effect on blood platelets. We investigated the effect of PA on human platelet aggregation using as PAs, staphylokinase (SAK), which has been found to have higher specific thrombolytic properties and less fibrinogenolytic properties than those of streptokinase, and also recombinant tissue-type plasminogen activator (TPA). Platelet aggregation was evaluated using platelet-rich plasma (PRP) or washed platelet suspension (WP). To examine the effects of PA, platelets were preincubated with PA (final concentration range: 0.001–100 μg/ml) at 37°C for 30 minutes. Both TPA and SAK inhibited platelet aggregation induced by collagen and ADP in PRP only at high concentrations (50–100 μg/ml). Both agents did not inhibit PRP aggregation induced by ristocetin. Although TPA and SAK did not inhibit platelet aggregation induced by collagen in WP which contained 0.5 mM calcium and 25 mg/dl fibrinogen, both agents inhibited aggregation under the same conditions in WP when the platelets had been preincubated with these agents and plasminogen (0.5 U/ml). The most effective concentrations were 100 μg/ml for TPA and 1 μg/ml for SAK. These effects were inhibited by adding aprotinin (1000 U/ml). We concluded from these results that, PA can inhibit platelet aggregation in WP by generating of plasmin and/or fibrinogen degradation products, but is only partially effective in PRP, possibly because of the existence of plasmin inhibitor.