Elevated plasma homocysteine is a risk factor for atherosclerotic disease. In the present study, we have examined whether the oxidative stress due to a low level of vitamin B 6 accelerates the development of homocysteine-induced atherosclerosis in rats. First, the effect of homocysteine thiolactone intake (50 mg/kg per d) on vascular integrity, lipid peroxide concentration, endothelial NO synthase (eNOS) expression and biochemical profiles was examined at day 1, day 21 and day 42 (five rats per group). The histochemical staining of the rat aorta showed no change at day 1 and day 21, but the subendothelial space was observed to be enlarged in rat aorta at day 42 with exposure to homocysteine thiolactone. Expression of eNOS was observed in rat aorta at day 42, but not at day 1 and day 21. Serum lipid peroxide concentration and biochemical profiles including glucose cholesterol and triacylglycerol showed no change at any day. Second, the effect of homocysteine thiolactone intake in the presence and absence of vitamin B 6 on vascular integrity was examined at day 1 and day 14 (five rats per group). Aortic lesions were observed in vitamin B 6 -deficient rat aorta at day 14 but not in vitamin B 6 -supplemented rats. The expression of eNOS was also observed in vitamin B 6 -deficient rat aorta at day 14. Serum lipid concentrations of the vitamin B 6 -deficient group significantly increased compared with concentrations of the vitamin B 6 -supplemented group, though serum concentration of homocysteine did not change between both groups. These results suggest that the oxidative stress caused by a low level of vitamin B 6 accelerates the development of homocysteine-induced atherosclerosis in rats.

The purpose of this study was to determine the effects of different exercises on skeletal muscle after ischemic reperfusion. [Subjects] Fifteen eight-week-old Wistar female rats were randomly divided into four experimental groups: normal, ischemic, light-exercise, and heavy-exercise. [Method] Ischemia was induced in the right lower limbs of the experimental rats. Exercise was started the day after ischemic reperfusion occurred. The relative weight ratios of the soleus muscles and the soleus muscle fiber cross-section minor axes were used for the evaluation of muscle atrophy. [Results] Compared with the ischemic group, the means of the soleus muscle fiber cross section minor axes significantly decreased in the heavyexercise group. [Conclusion] Our results suggest that heavyexercise after ischemic reperfusion of the skeletal muscle may cause muscle atrophy.

Based on the conclusion of our previous report, we performed follow-up angiography on the 61 outpatients who had undergone neck clippings for cerebral aneurysms more than 5 years ago.According to the findings of the original angiograms, they were classified into 4 groups: Group 1 consists of 34 cases without abnormal finding. Group 2a consists of 14 cases with small, unruptured aneurysms, that were too small to operate on. Group 2b is 10 cases with residual aneurysmal necks

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