1. Enzymes from culture filtrate of a strain of Clostridium terlium which decomposes A, O(H), Le^a, Le^b and pneumococcus Type X IV specifities in blood group substance were purified by fractionation with ammonium sulfate (4050%) and acetone (050%), following column chromatography on DEAE-Sephadex A-50. A-destroying enzyme preparation was eluated from the column with pH of 6.8, 0.02M. of phosphate buffer. Enzyme preparation destroying O(H), Le^a, Le^b and pneumoccus Type X IV antigenicities was obtained in a fraction on rechromatography, eluated with 0.47M of sodium chloride in pH 6.8, 0.02M of phosphate buffer.
2. This enzyme preparation digested O(H) +, Le(a±b+) and Le(a+b-) substances to release fucose, galactose and N-acetylglucosamine but not N-acetylgalactosamine do. According to the results, the enzyme preparation is considered to function as (α-) L-fucosidase, (β-) D-galactosidase and (β-) N-acetyl-D-glucosaminidase.
3. In dialysates of O(H), Le(a±b+) and Le(a+b-) substances digested by the enzyme preparation, molecular ratio of fucose : galactose : N-acetylglucosamine is respectively 3 : 3 : 2 and 1 : 2 : 2. Fucose and galactose are liberated about 70% and 60% of total amount of fucose and galactose, respectively in former, and also about 40% and 45% of total amount of each of these sugars, respectively in latter. N-Acetylglucosamine liberated in both of these dialysates is nearly 50% of total amount of N-acetylglucosamine, finding scarecely difference between them.
4. There is known to be present fucose, equivalent to about 7% of anthrone-tryptophan value in both of these non-dialysates, which is irresponsible for antigenicities in O(H), Le^a, and Le^b. O(H) antigenicity is digested by the enzyme preparation more rapidly than pneumococcus Type XlV antigenicity in O(H) +, Le(a±b+) substance.
5. Galactose and N-acetylglucosamine are recognized to be responsible for determinant group of pneumococcus Type XIV common antigen in blood group substances. In addition, based on the results presented, quantitative relationship among O(H), Le^a, Le^b and this antigen was discussed with a proposal of basic inner structure in soluble blood group substance.

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The chemical action of purified Le^a decomposing enzyme preparation from Bac. cereus on the water-soluble Le^a and O(H) substances has been examined. Besides β-galactosidase, this enzyme preparation contains α-fucosidase which is different from that in O(H) and Le^b enzyme preparation from Bac. fulminans or Bac. cereus O(H).
1) Le^a enzyme preparation acts on Le^a substance to leberate about 34% of the original fucose and 32% of the original galactose as simple sugars.
2) Le^a enzyme preparation acts on O(H) substance to liberate fucose and galactose as simple sugars amounting to 3% and 19% of the original quantities respectively. Subseqent treatment with O(H) and Le^b enzyme preparation from Bac. fulminans appears Le^a activity and liberates from the Le^a enzyme treated substance 32% of the original fucose and 2% of the original galactose as simple sugars. The third treatment with Le^a enzyme preparation destroys newly developed Le^a activity and liberates fucosc and galactose as simple sugars amounting to 28% and 8% of the original quantities respectively.

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This report deald with the “special type” of hepatocerebral disease, a 57 aged woman who had been suffered from repeated attacks of loss consciouse under the signs of latent liver insufficiency and died about five years after the onset of symptoms.
Autopsy disclosed atrophic fibrosis of the liver, enlargement of the spleen and swelling of the brain.
Microscopically the changes in the liver were characterized by irregular degeneration of the hepatic cells associated with fibrosis and lymphocytic infiltration.
The normal architectural arrangement of lobules was markedly distorted. The changes in the brain consisted of spongy vacuolation of the white matter and varying degrees of degeneration of the nerve cells associated with an appearance of so-called Alzheimer's “nackte” glia.
The process was found diffusely thoughout the brain. From the combined degeneration of the brain and the liver, and the characteric clinical features, this case is summarized as INOSE's type of hepato-cerebral disease. No evidence with etiological significance was demonstrated in this case.

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The following are results of clinical observations made with 93 patients of jaw bone fracture who visited our clinic during a 7 year period from 1957 to 1963.
1) Patients with jaw bone fracture had abruptly been increased since 1962.
2) Male patients were far more numerous than the female.
3) As for the age, the incidence rate was higher in 2130 years. It was, however, noteworthy that the fracture was observed relatively often among children of below 10 years.
4) As for the cause, traffic or work accidents were numerous.
5) As for the incidence rates by months, the greatest number occurred in May, and the smallest in December, and the number in the morning was smaller than that in the afternoon.
6) Fracture of the mandible was oftener than that of the maxilla, and it was apt to occur in the median, canine teeth region and wisdom teeth region to the terminal angle. In the maxilla, the median part was most easily afflicted.
7) Recently, complicated fracture has increased in proportion, and the fracture is becoming more and more complicated.
8) We must take care for frequent side injuries such as damage in facial soft tissue and for sequel such as numbness in the labial region.
9) The interval between the incidence of the fracture and commencement of clinical treatment was generally within 10 days.
10) As for the treatment, application of the Sannai's splint in association with the kin cap was effective. When operative restoration was necessary, the majority were treated successfully by bone suture using 18.8 steel and silver wire.
11) By use of anabolic steroid hormone, body weight gain could be obtained more satisfactorily than with amino acid preparations, and subsequently days of treatment could also be reduced.
12) A case which had received inadequate treatment was rentgenographically presented with the object to explain our method of treatment which we consider appropriate.

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Intraventricular administration of 25μg/kg of adrenaline induced consistently a delayed rise in gastric pepsin output in the Heidenhain pouch dog, wich is referable due to the release of ACTH. This response was blocked by pituitary stalk section and also significantly suppressed in pepsin output by electrolytic lesions placed in the median eminence and posterior hypothalamic regions.
Ten μg/kg of adrenaline injected into the median eminence and posterior hypothalamic regions. caused a significant increase in gastric pepsin secretion, while the same dose of adrenaline injected into the anterior hypothalamic regions failed to do. An intrahypophysial injection of 25μg/kg of adrenaline, either into the anterior or the posterior lobe, proved ineffective.An intracarotid injection of 100μg/kg of adrenaline had no stimulatory effects on gastric secretion.

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