Prototype strain, M-25, of parainfluenza type 4 (PI-4) virus was grown to high titers and passaged serially in Vero (Cercopithecus kidney cell line) cell cultures under fluid overlay containing low concentrations of trypsin. Infectivity titers in both primary cercopithecus kidney cell cultures (VK) and in Vero cell cultures under ordinary conditions (Vr^o) did not change essentially through passages in the trypsin-added Vero cell cultures (Vr^t) from those of the original VK-grown virus. The 14th Vr^t-passage virus was not transferable in Vr^o beyond two subpassages. Consequently, occurrence of adaptation to Vr^o during passages in Vr^t can be excluded. Identification of Vr^t-grown virus as PI-4 was demonstrated by the cross neutralization and hemagglutination-inhibition tests performed among paramyxoviruses and by several biological and physico-chemical tests. Other proteolytic enzymes, pancreatin and pronase, gave similar results as did trypsin, but hyaluronidase and lysozyme were ineffective. It was found that animal sera were inhibitory to the trypsin-effect mentioned above. Therefore, the Vr^t system must be serum-free for obtaining reproducible results.

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Serological properties of 468 strains of the cholera group of vibrios, in which cholera and NAG vibrios are included, were studied. The results are summarized as follows:
1. By cross agglutination tests, 39 O groups of which O group 1 was assigned to cholera vibrio were established within the group.
2. It was demonstrated that H antigen of the cultures of all O groups was identical with that of cholera vibrio but was different from that of other species of the genus Vibrio.
3. The mucoid antigen which inhibits O agglutination was found in some strains.
The results support the findings of Gardner and Venkatraman. In addition, it was emphasized that the O groups established in this study should be referred to as serotypes within Vibrio cholerae including NAG vibrios, since all the strains of this species possessed a common H antigen.

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The immunogenicity of α toxoid resided not in the residual undenatured toxin but in the toxoid itself. The toxoid preparations derived from purified toxin showed a high immunogenicity in guinea pigs, while those prepared from crude toxin a low immunogenicity. It was indicated, however, that the immunogenicities to rabbits were on the same level. It is discussed that α toxoid from purified toxin may be useful in the prevention of human gas gangrene, but κ antigen may be less important.

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Azo-dye was liberated from azocoll not only by proteolytic enzymes but also by albumin (serum or egg), a culture medium (papain digest of meat) or polyvinylpyrrolidone (PVP) . Pretreatment of azocoll with papain and PVP increased the reactivity of azocoll to κ-toxin of Clostridium perfringens. A rapid and reliable assay method of κ-toxin and κ-antitoxin using the pretreated azocoll is described.

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Intravenous injection into the rat of the lymphocytosis-promoting factor (LPF) caused a striking leukocytosis characterized by predominant small lymphocytes. The lymphocytosis appeared as early as 3 hr after the administration of LPF.
The mechanism of the lymphocytosis with LPF in the rat was investigated under the current knowlege of the lymphocyte recirculation by the thoracic duct drainage technique.
The lymph flow and the lymphocyte output from the thoracic duct drainage were almost completely blocked several hours after the LPF injection without any period of apparent augmentation in lymphocyte output, while the number of peripheral lymphocytes continued to increase as did the LPF-inoculated rats having no thoracic duct cannula. The evidence suggested that the entry of lymphocytes from the lymphatic tissues into the blood stream via the so-called direct route was enhanced by the LPF administration. The size of increase, however, was so small that the lymphocytosis was not attributable to the increase in the lymphocyte output via the direct route. On the other hand, the lymphocytes treated in vivo or in vitro with LPF did not migrate from the blood stream into the lymph nodes when transfused into normal rats.
These are the evidences to show that the lymphocytosis induced by LPF is due to the modified recirculation of lymphocytes as a result of direct effect of LPF on small lymphocytes. The affected lymphocytes lose the capacity to go back from the blood stream to the lymph nodes. There is no evidence of increase in the rate of entry of lymphocytes from the lymph nodes into the blood stream.

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