Investigation of the Lewis blood group was carried out on 485 persons with anti-Le^a, anti-Le^b, and anti-Le^c antibodies which were obtained by immunizing the rabbit with human saliva, with the following results: Le(a+b-c-) cases numbered 107(22.06%), Le(a- b+c-) cases 369(76.08%), and Le(a-b-c+) cases 9(1.86%). Le(a+ b-c-) cases belonged to non-secretors, and Le(a-b+c-) cases secretors, whereas Le(a-b-c+) cases belonged to secretors except one non-secretor.
The results of investigation of families containing Le(a-b-c+) members indicated that the gene Le^b is dominant against the gene Le^a, and that the gene Le^c is dominant against the genes Le^b and Le^a. Consequently, the genotype for Le(a+b-c-) is considered to be Le^aLe^a, and as the genotypes for Le(a-b+c-), Le^aLe^b, and Le^bLe^b, and for Le(a-b-c+), Le^aLe^c, Le^bLe^c, and Le^cLe^c can be distinguished. The frequency of each gene for Japanese was as follows: Le^a, 0.4697; Le^b, 0.5210; and Le^c, 0.0093.

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The influence of bacterial adrenaline sensitizer (B.A.S.) in the establishment of damages to arteries and heart caused by adrenaline administration was analysed in rabbits.
B.A.S. used in this experiment is a polysaccharide fraction prepared from a cell body of Shigella flexneri 2b isolated from a patient with “le syndrôme malin” of Ekiri.
20 rabbits were fed on low fat diet of barleycorn and vegetables and divided into 4 groups, each consisting of 5 animals. In group A 25γ/kg adrenaline alone was administered intravenously every 2 days. In group B 25γ/kg B.A.S. alone and in group C 25γ/kg adrenaline combined with 25γ/kg B.A.S. was administered intravenously every 2 days. Group D was the control. After 3 months all animals were sacrificed for pathological observations.
All animals treated with adrenaline showed Monckeberg's arteriosclerosis in aorta, proliferative endarteritis in medium and small-sized arteries, and myocardial infarction in left ventricle.
The change of arteries is striking specifically in the coronary arteries of the wall of left ventricle, especially in medium-sized artery, showing a strong thickening of the intimal layer and also the strong narrowing of the blood vessel lumen due to endarteritis proliferans.
The fat deposition in the intima of aorta was observed in animals treated with B.A.S. alone, with adrenaline alone, and with the combina tion of B.A.S. and adrenaline.
The strongest change of aorta of Mönckeberg's type and the most marked fat deposition in the intima of aorta were observed in animals treated with the combination of adrenaline alone and B.A.S. But between the fat deposition in the intima and the damages of the media there was no correlation.
Adrenaline and noradrenaline, so noxious hormones under the influence of B.A.S. to the artery, especially to the coronary artery of the left ventricle, must be reexamined as a factor causing human arteriosclerosis and myocardial infarction in connection with the cholesterol atheromatosis.

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