The oncogenic effect of dimethylnitrosourea (DMNU) was investigated in rats of Donryu strain. The tumor induction was made in two ways. In the first experiment, 40mg of DMNU per Kilogram of body weight were given weekly to adult rats at 6weeks of age by tail vein injection up to a total dose of 211 to 250mg. In the second experiment, a single dose of 50mg of DMNU per Kilogram was administered intravenously to pregnant rats of the 20th day of gestation.
In the first group, 30 animals had survived into tumor bearing age, among which 26 were found with a total of 45 tumors. Nervous system tumors amounted 42, comprising 90.3% of the total number of neoplasms. In the second group, of 31 litters treated with DMNU through the mothers, 21 developed tumors. Of a total of 23 tumors, 14 were produced in the Kidney, 8 in the nervous system and 1 in the breast. Organtropism of the carcinogenic effect of DMNU appeared shifted toward prevalent induction of Kidney tumors in rats when treated during pregnancy.
The nervous system tumors produced in both experiments amounted 50, among which 3 were produced in the brain, 1 in the spinal cord, 6 in the cranial nerve, 38 in the spinal nerve root and 2 in the peripheral nerve. The prevalent induction of nerve tumors in the spinal nerve roots and peripheral nerves in rats exposed to DMNU appears similar to previously reported distribution pattern of neurogenic tumors induced in rats by methylnitrosourea (MNU).
Acording to the cytology and pattern of predominant neoplastic cells, tumors of the brain and spinal cord were classified into 3 types ; mixed glioma, anaplastic astrocytoma and oligodendroglioma. Mixed glioma showed an irregular admixture of neoplastic astrocytes and oligodendroglioma. In electron microscopy, neoplastic astrocytes appeared dark with blunt processes which contained variable numbers of glial filaments and microtubules. Oligodendroglial cells displayed an electron lucent cytoplasm which was poor in organellas. Some of the cells with clear cytoplasm also contained masses of glial filaments,
Microscopic appearance of nerve tumors produced was that of anaplastic neurinoma. The electron microscopy of component cells was characterized by the presence of interdigitating cell processes, intracellular filaments, cell junction of intermediate type, occasional incorporation of axons, and of a partial basement membrane. The majority of nerve tumors examined were considered to originate from Schwann cells. Aldorase and LDH isozyme pattern were investigated in a solitary passaged nerve tumor together with normal rat brain. The enzyme activities specific for brain were not detected in the transplantable nerve tumor.

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汎発性鞏皮症20例の前腕および背部皮膚のコラーゲン合成活性を石川の組織学的病期分類に従って分類し, その変動を検討した.コラーゲン合成活性は採取皮膚を細切後³H-proline含有培養液中で培養後その³H-hydroxyprolineをJuva-Prockopの方法にて測定した.さらに汎発性鞏皮症患者尿より分離したムコ多糖画分より惹起した実験鞏皮症マウス皮膚についてもコラーゲン合成活性を検討した.
1. 汎発性鞏皮症におけるコラーゲン合成活性は臨床的無疹部 (stage I) の皮膚では亢進を認めず, 硬化性病変が初まるstage IIにおいて初めて, その一部に合成活性の上昇をみ, 硬化病変の完成するstage IIIでは再び正常皮膚と同じか, むしろ低いコラーゲン合成活性を観察した.
2. 実験鞏皮症マウスでは発病因子を腹腔内, 局所注射したいずれにおいても組織学的に明らかな皮膚硬化がみられなかったマウスの一部においてコラーゲン合成活性の亢進を示すものがみられた.しかし, 明瞭な皮膚硬化を示した皮膚では合成活性の亢進を示すものはなかった.
すなわち, 汎発性鞏皮症皮膚のコラーゲン合成活性はその病期に依存し, stageIIの合成活性の亢進よりもstageIIIの合成活性が上昇していない事に意義があり, 実験鞏皮症でもほぼ同様の傾向をみとめた.これらの結果から汎発性鞏皮症皮膚病変におけるコラーゲン合性活性の亢進は一過性にすぎないと推定される.

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The presence of two precipitins against blood group H substances from human gastric linings and ovarian cyst fluids was demonstrated in natural eel serum by immunodiffusion techniques in agal gel. One of them which form the precipitation band to antigen side was the known anti-H precipitin containing anti-H agglutinin activity. Reaction of the anti-H precipitin with H substance was inhibited by L-fucose. This anti-H precipitin reacted well with H substance from hog gastric linings but did not show clear precipitation bands with H substances from saliva, meconium, semen and intestines. The other precipitin which form the precipitation band to antiserum side in agar gel reacted well with H substances from human secretions and tissues but not reacted with hog H substances from gastric linings and submaxillary gland. This precipitin did not agglutinate O red cells and was not absorbed by O red cells. The reaction of the precipitin with H substances was not inhibited by L-fucose. Because this precipitin reacted with water soluble H substances from human “secretor”, the antigen named H (Se) and antibody anti-H (Se).

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This paper reported on a follow-up of 43 children diagnosed as “non-attendance at school” during past eleven years (1964-1974) in our outpatient clinic.
We obtained following results.
1) These children could be divided into 19 acute and 21 chronic cases by their pattern of absence.
2) Generally, acute type had good prognosis and chronic type had poor one.
3) Poor prognosis of chronic type might be improved by persistent efforts of key-person or admission.
Detailed case reports on therapeutic approach will be demonstrated in the next paper.

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In order to clarify the induction mechanism of the late cutaneous allergic respose (LCAR), the following were studied : 1) intracutaneous test with various kinds of allergens, 2) reversed type allergic resposes using anti-human IgE rabbit serum (aIgE), 3) P-K tests with several antigen-anti-body systems. Histopathological study of skin sites showing positive LCAR was performed. The following results were obtained :
1) The frequency of LCAR varied with the kind of allergen used. The type of LCAR (isolated or dual type ; immediate and late) depended on the kind of allergen.
2) Intracutaneous injection of aIgE also induced LCAR. There was no significant difference in the frequency of the response asthmatic patients and healthy volunteers.
3) LCAR was often detected 4-8hours after the immediate reaction in P-K tests. However, in some cases LCAR was observed in negative P-K tests.
4) Histological findings of LCAR showed edema in dermis, swollen collagen fibers and invasion of lymphcytes and polymorphnuclear leucocytes around blood vessels.
5) No correlation between the frequency of LCAR and IgE levels in the blood of the asthmatic patients was observed.

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The present case was a 24-year-old man with hereditary factor. He was the offspring of a consanguineous marrige between cousins. His brother died of the same disease at the age of 29 years. The youth developed well physically and mentally. The first convulsive seizure occured at the age of 15. He developed an ataxic gait, speech disturbance, dementia and myoclonic jerks were noted occasionally in the face and extremities. Convulsive seizure occured very frequently despite anticonvulsant chemotherapy.
He gradually fell into severe dementia, was bedridden and totaly incontinent. He died after about 9 years from the onset.
Histopathologically the Lafora-body was found in all areas of the brain, especially in the substantia nigra, the nucleus dentata cerebelli, globus pallidus and occipital lobe. The degenerative substance was found in the myocardium and liver cells.
Electroencephalographical, histopathological, electronmicroscopical and biochemical investigation were carried out in this case. Clinicopathologically, it revealed a typical myoclonus epilepsy (Lafora-body type).
Regarding about pathogenesis of Lafora disease, polyglucosan metabolism disorder was discussed.

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A 1000-fold purification of anti-A hemagglutinating lectin from Falcata japonica was obtained by means of ammonium sulfate fractionation, gel filtration of Sephadex G-100 and affinity chromatography on N-acetyl-D-galactosamine-starch. The isolated lectin formed a single diffuse band in polyacrylamide gel electrophoresis and has an approximate molecular weight of 120, 000 as estimated by measurements of Sephadex G-200 gel filtration and ultracentrifugal analysis. The lectin was rich in asparatic acid, serine and glycine. Trace of methionine was detected but no cystine was found.

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