In order to investigate the role played by the different organs of chicken red blood cell (for example, Nucleus, Mitochondria, Microsome, etc.) in hemoglobin formation, several experiments were carried out.
The results were as follows :
1) The biosyntheses of porphyrin and heme were observed in each fraction of chicken red blood cell, however, concerning the ability of biosynthesis of protoporphyrin in the supernatant fraction, a conclusion was suspended.
2) In 1000g fraction of chicken red blood cell uroporphyrin and coproporphyrin were formed at first and then protoporphyrin : in 10000g fraction uroporphyrin only was produced at first : in 20000g fraction and the supernatant fraction, the three porphyrins were simultaneously obtained from the onset.
3) KCN (10^-4M, 10^-3M) remarkably inhibited porphyrin and hem formation in 1000g and 10000g fractions respectively, and RNA ase (0.5mg/ml) prevented porphyrin and heme formation only in 10000g fraction. Pb, (CH₃COO) ₂ (10^-4M, 10^-3M) obstructed protoporphyrin formation and incorporation of iron into heme, especially in 1000g fraction and CoCl₂ (10^-4M, 10^-3M) inhibited porphyrin and hem formation remarkably, having no direct erythropoietic faculty. Folic acid (15mg/10ml) accelerated porphyrin formation especially in 1000g and 20000g fractions, while it inhibited heme formation conversely, VB₁₂ (30γ/10ml) stimulated porphyrin synthesis only in 1000g fraction, having no effect on heme synthesis. ATP (10^-2M), orotic acid (10^-2M) thioctic acid (10^-2 M), ACTH (25^I.U./10ml) etc, did more harm than good.
4) The X-Ray inhibited the biosynthesis of porphyrin in all the fractions, especially at above 1000γ and protoplasmas were more influenced in heme biosynthesis.

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In order to study the morphogenesis of atherosclerosis, human aortas at various ages from embryo to 86 years were investigated pathologically, pathohistologically and histochemically. At the same time, experimental atherosclerosis in cholesterol-fed rabbits which were bred in normal stock diet for 18 months afier cessation of cholesterol feeding were compared with those of human subjects. Further in order to examine the thrombogenic theory concerning genesis of atherosclerosis, reduplicate observation was made by Duguid method.
1) Intirnal thickening of the human aorta with ageing was observed from embryonal stage.
2) Arteriosclerosis of the aorta was remarkable in the abdominal aorta which showed great development of intima with ageing, and was mild in the ascending aorta which showed weak one. Consequently it is considered that a common factor may be involved both in diffuse intimal thickening with ageing and development of atherosclerosis.
3) Atherosclerosis is observed approximately at age above 50, but it appears ten years earlier in the hypertensives.
4) The early lesion of arteriosclerosis is intimal edema; atherosclerosis develops from it by insudation of blood plasma rich in lipid and fibrous plaque is produced from it when is is poor in lipid.
5) The precursor of atherosclerosis is intimal lipoidosis (fatty streaks or fatty spots). Lipid accumulated in the intima consists of lipid insudated directly from the circulating blood and of cellular lipids (foam cells and smooth muscle cells).
6) Pathohistologically, there are two types of atherosclerosis-type α which mainly consists in fatty swelling of collagen fiber and type β which mainly consists in tissue debris. The type α develops when intima contains poor lipids and rich collagen fibers and the type β is produced when it contains rich lipids and few collagen fibers. Foam cells play a very important role in the formation of type β atherosclerosis.
7) In order to investigate the significance of thrombi in the morphogenesis of atherosclerosis, the aortas of 50 autopsy cases ranging in age from 10 to 81 were studied. There were, however, no findings which indicate that thrombus played a principal role in the morphogenesis of atherosclerosis.
8) The rabbit which was first raised on 1 per cent cholesterol diet for 14-17 weeks and then on normal stock diet for 61 weeks at the longest, showed the closely slmilar change-to human atherosclerosis, especially of type β.
9) In the rabbit raised by the daily administration of the diet containing 6 g lard for a year, atherosclerosis does not appear. Therefore neutral fat is not involved in the formation of atherosclerosis, but the participation of cholesterol has an important significance.

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1. The blood group A-decomposing enzyme preparation from Clostridium tertium A which had been adsorbed on a DEAE-Sephadex column was eluted in two portions which had A-decomposing activity. The fast eluted fraction (Fr. 4) had activity of N-deacetylase, and when incubated with A substance, it abolished the A-activity, which was restored by N-acetylation. It did not abolish the reactivity of A substance to anti-A+B agglutinin of group O serum or of plant seed, nor it affected the O (H) -activity. The slow eluted fractions (Fr. 31- 34), acting on A substance, destroyed its A-activity and reactivity to anti-A+B agglutinin, and enhanced O (H) -activity. In this case, the lost A-activity of the ènzyme treated substance did not restore by N-acetylation.
2. Antiserum, prepared by immnizing the rabbit or chicken with Fr. 4-treated A substance, contained an antibody which reacted with Fr. 4 -treated blood group A red cells but not with untreated blood group A or B red cells and blood group substances, and which was specifically inhibited by D-galactosarnine. When incubated with Fr. 31-34 enzyme, the Fr. 4- treated A substance or red cells lost reactivity to this antiserum, while the O (H) -activity was enhanced.
3. Fr. 4 of A-decomposing enzyme did not liberate reducing sugar from A substance or blood group A red cells, whereas Fr. 31-34 of A-decomposing enzyme freed galactosamine (and a small amount of N-acetylgalactosainine) from them. These results show that Fr. 4 exerts N-deacetylase action on N-acetylgalactosaminoyl residue, which is determinant of the A specificity, and that Fr. 31-34 possesses the activity of galactosaminidase and/or partially of N-acetylgalactosaminidase as well as the activity of N-deacetylase.

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Surveys of staphylococcal strains, isolated from clinical sources, disclosed the follwong facts : Multiple resistant strain wiht special reference to tetracycline, streptuiycin, sulfanilamide, and penicillin, were manifest and they were restricted to specific phage group.
Allmost all of the strains resistant to penicillin, were found to be capable of produing penicillinase. The relation between penicillin resistance and activity of penicillinase formation was studied, penicillin resistance of naturally occurring strains and that of the strains developed in lavoratory were compared, the forming penicillinase and the latter do not.

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The naturally occurring strains of staphylococci resistant to chloramphenicol inactivate the drug through acetylation. The loss of resistance to chloramphenicol on aging was accompanied by the loss of capacity to inactivate the antibiotic. The chromatographic behavior of the product of chlorarnphenicol, inactivated by chloramphenicol-resistant staphylococci, was found to show 3-acetoxy chloramphenicol.

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An autopsy case of typical systemic lupus erythematosus accompanying conspicuous angitis was reported. A 34 aged woman was admitted to a hospital with chief complaints of erythema, pyrexia, arthralgy, edema and proteinuria, and finally she died of renal failure about 8 years after the onset of symptoms.
Histologically, diagnosis of systemic lupus erythematosus was confirmed by typical wire-loop lesions, onion-skin lesions and Libman-Sacks endocarditis. It was interest to note that angitis was found in general organs. Small-and medium-sized arteries showed various stages of arteritis, namely a) fibrinoid degeneration of the intima and b) cellulo-fibrous intimal thickening without granuloma formation in the adventitia.
It may be considered that this case was systemic lupus erythematosus accompanying marked angitis as a result of prolonged process or the modification of lesions achieved by steroids.

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In July 1966, an outbreak of an acute gastroenteritis-like illness in a children's dub in Gumma Prefecture, and 51 cases were reported.
Clinical and epidemiological features of the disease were similar to that of food poisoning. However, no causative agent was detected from stools or blood samples by bacteriological examination.
In monkey kidney cell cultures 2 strains of Coxsakie A9 virus were isolated from feces of 6 cases, and antibody to this agent was demonstrated in the sera collected from the patients both by complement-fixation tests and neutralization tests.
Available evidence indicated that the disease was presumably due to Coxsakie A9 virus.

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