Abstract. Because ADP has been reported to produce a secondary wave of platelet aggregation in diabetic subjects, and since ADP is known to enhance normal platelet biosynthesis of pro‐aggregating thromboxane A2, we tested whether or not the reported increased sensitivity of diabetic platelets to ADP may also result in increased platelet biosynthesis of thromboxane A2. To test this hypothesis, 14C‐arachidonic acid (14C‐AA) was incubated in vitro with washed human platelets' in the presence or absence of ADP. These studies included platelets isolated from thirty normal volunteers, twenty‐six diabetic subjects with and without known vascular complications, eighteen non‐diabetic pregnant females and fourteen pregnancy‐induced diabetic females. Data from these studies demonstrated: (i) a significant increase in the capability of diabetic platelets in response to ADP to biosynthesize thromboxane A2 from arachidonic acid when compared to platelets from normal controls (P < 0.001); (ii) a significant increase in thromboxane A2 biosynthesis by platelets from pregnancy‐induced diabetic subjects over nondiabetic pregnant females (P < 0.001); (iii) a two‐fold increase in thromboxane A2 biosynthesis by platelets from diabetic subjects with vascular complications when compared to those without vascular complications. Although our data also showed approximately a twofold increase in thromboxane A2 biosynthesis by platelets from diabetic subjects with greater than 10 years of the disease when compared to diabetic subjects with less than 10 years, these latter results were, however, not statistically significant. Results from these studies suggest that a relationship may exist between the markedly increased ADP‐induced platelet aggregation in diabetes mellitus and the vascular complications associated with this disease. Whether or not increased capacity of the diabetic platelet to biosynthesize pro‐aggregating thromboxane A2 in response to ADP or other pro‐aggregating agents is per se a triggering factor in occlusive vascular diseases reported in diabetic subjects must await further studies.

High temperature fatigue crack growth behavior of silicon nitride has been investigated. Fatigue crack growth resistance decreased with increasing temperature and with decreasing loading rate at high temperature above the glass softening temperature. Microvoids were nucleated at triple points due to grain boundary sliding in the near crack tip region. The microvoid grew along a grain boundary accommodated by sliding of the adjacent boundaries to form a microcrack. A fatigue crack propagated by coalescing to the microcracks. The stress shielding due to bridging formed in the crack wake had also a significant influence on the fatigue crack growth behavior at high temperature.

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A 46-year-old housewife was treated orally with 5-fluorocytosine (5-FC). She was almost cured at 15 weeks after the administration. Under histological and electron microscopical examination, spores in the lesions were observed to be markedly decreased in number, and all of them had suffered a change of shape or had been destroyed. At the end of 33 weeks, however, the patient had a complete relapse.

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