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Electromigration-induced failure mechanisms were investigated by means of extremely sensitive resistance change measurements and simultaneous observations using scanning electron microscopy. Abrupt changes in resistance ( ACRs), classified into three types: downward steps, upward steps, and oscillations, were found to occur frequently during the dc current stressing test. It was conspicuously observed that there was a rapid void annihilation associated with an abrupt increase in resistance, and a rapid void formation with a decrease in resistance. ACRs are considered to be caused by a rapid change in the number of excess vacancies concomitant with void annihilations or formations. The thermodynamical analysis on the stability of a void strongly suggests that the change of a local stress from tensile to compressive causes a rapid annihilation of voids, and the opposite one causes a rapid formation. Temperature dependence of the intensity of ACRs exhibited an activation energy of 0.43 eV, which implied that grain boundary electromigration was the driving force of ACRs.

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in leukocyte migration from the circulation and intervention at sites of inflammation. We investigated the effects of various types of exercise on circulating levels of soluble ICAM-1 (sICAM-1) in normal healthy male adults. Plasma concentrations of sICAM-1 were measured before and after bicycle ergometer exercise at intensity of 80% maximal oxygen consumption (VO2mag) (16 min), 42 km endurance running and 30-min downhill running at intensity of ventilation threshold (VT). The plasma sICAM-1 level increased 1 day after the endurance running (12%) and downhill running (14%), but not after ergometer exercise. Plasma C-reactive protein (CRP) and creatine kinase (CK) concentrations also increased 1 day after running. Our data suggest that exercise associated with muscle damage and/or inflammation results in increased levels of plasma sICAM-1. The physiological significance of post-exercise high plasma sICAM-1 levels is not clear at this stage, but changes in plasma sICAM-1 may reflect the status of the immune system.

Weexamined the relationship between left ventricular hypertrophy (LVH) and renal and retinal damage in 174 untreated patients with essential hypertension. As an index of renal and retinal damage, we examined proteinuria and retinal vascular change. LVH was diagnosed according to left ventricular mass obtained from echocardiography. Of the hypertensive patients, 111 patients (64% ) had LVH. The incidences ofproteinuria and advanced retinal vascular change werehigher in patients with LVH than in those without LVH. In a multiple regression model, there wasa significant positive correlation between left ventricular mass and proteinuria, as well as diastolic blood pressure, sex, age and body mass index. In conclusion, proteinuria is related to elevated left ventricular mass in patients with essential hypertension.