Chloramphenicol-sensitive, -resistant, and -temperature-sensitive R factors obtained from a chloramphenicol-resistant R factor (NR1) were characterized. The transfer frequency of the chloramphenicol-sensitive R factors was variable. The mechanisms underlying this variability are unknown. The chloramphenicol-sensitive-R-factor strains produced at a low frequency chloramphenicol-resistant revertants, some of which were temperature-sensitive to chloramphenicol. These R factors were not eliminated at 42 C indicating that the temperature-sensitive mutation is due to the mutation of the chloramphenicol resistance gene of the R factors. Survival of E. coli K12 carrying the chloramphenicol-temperature-sensitive R factor as a function of chloramphenicol concentration and of temperature was investigated. The growth of E. coli K12 carrying the R factors on chloramphenicol-containing agar plates was inhibited at 40 C or higher temperatures.
Two chloramphenicol-sensitive R factors were of high-transmissible mutant types, and transferred chromosomal genes at a higher frequency than the original R factor, NR1. The bacterial strains carrying the R factors were sensitive to phage f2. From one of them, we isolated episomes which had properties similar to the F factor and had lost all the drug-resistance genes. These episomes were designated as F-like factors. The F-like factors, probably derived from the R factor, were indistinguishable from the F factor except that the F-like factors transferred chromosomal genes by the mixed cultivation techniques at a slightly lower frequency than the F factor.

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Antibodies against reovirus types 1, 2 and 3 were detected in dogs, swine, race-horses, and wild rats at certain rates for each serotype of the virus.
Judged from the results of our serological examinations in those animals, each species of animal seems to have its own epidemiologic characteristic more or less for each of the three serotypes.
There seem to be two groups of mammals according to their epidemiological behavior to the reovirus infection. In one of the groups, the infection is established in a considerably early period from birth, for instance in swine, while in the other group animals become infected in a much more delayed time and a considerable portion of them remain uninfected till a long time after birth, as in the case of dogs, horses, or wild rats.
In wild rats, an epidemiological wave was recognized as judged by a sudden appearance of reovirus antibodies in a herd.

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The lymphocytosis-promoting factor (LPF) was found to suppress the formation of circulating antibody in mice at various immune stages.
The primary immune response of mice to sheep red cells (SRC) was suppressed to a marked extent when LPF was inoculated 1, 2 or 3 days before the antigen. Not only the formation of both 2-mercaptoethanol-sensitive and -resistant serum hemagglutinins was delayed but also the peak titers were reduced. The smaller the dose of the antigen to immunize the LPF-pretreated mice, the more pronounced was the effect. Some data suggested that the pretreatment with LPF one day prior to the antigen was the most effective, but the results were not consistent.
The primary immune response to tetanus toxoid was also suppressed. When LPF was administered 3, 4 or 6 days prior to the antigen, the suppression was significantly greater than when it was given 1 or 2 days before the antigen.
The secondary antibody production to SRC was also delayed and the titer was lower than that of control.
The mice deprived of the primary response to SRC by the LPF pretreatment did not show the secondary type response to a subsequent inoculation of SRC. This shows that no immunological memory was conferred by the primary inoculation of the antigen.
The mechanism of the immunosuppression by LPF is discussed on the basis of these findings as well as in light of the current views concerning the mechanism of antibody formation.

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When typhoid vaccine was injected to Clonorchis sinensis infestated guinea pigs, the titer of the H-agglutinins in response to the injection was reduced in the infestated animals as compared with the uninfestated controls. Moreover, the heavier the infestation the lower was the agglutinin response. It was suggested that compression of the liver cells by the fibrosis around intrahepatic bile ducts as a result of the infestation contributed to the variation in antibody response in the infestated animals.

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Epidemiological analyses on the preventive effect of thiabendazole as an ovicide against human helminth infections are described. Thiabendazole was mixed in night-soil once a month during a period from April to October 1964 in the control of hookworm infection, and from June 1964 to March 1966 in the control of Ascaris and Trichuris infections. The findings are as follows: (1) The rate of new infections with hookworms (Necator americanus) in the treated area was two fold lower than that in the non-treated area. (2) The rate of new infections with Trichuris in the treated area was three fold lower than that in the non-treated area. (3) As to the new infections with Ascaris, the rate of patients with fertilized eggs in the treated area was four fold lower than that in the non-treated area. Moreover, new infections were found to occur in groups in the families of the non-treated area, whereas the incidence was sporadic in the treated area.

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