The organochlorine pesticide residue in diet for laboratory animals was quantitatively determined by gas chromatography with acetone and n-hexane extracts. The total level in the diet for mice and rats was 0.243 ppm when determined in June, 1970 and 0.044 ppm in June, 1973. Of the pesticides detected in the diet, α-BHC level greatly varied depending upon years, being 0.081 to 0.141 ppm in June, 1970 and 0.009 ppm in June, 1971, while β-and γ-BHC levels showed little changes. The pp' DDT level was much lower in 1973 than in from 1970 to 1972. No or only little aldrin and endrin were detected throughout the period of investigation (1970-1973) . Similar results were obtained also with the diet for dogs, rabbits, monkeys and chicks. The level of total organochlorine pesticide was detected higher in wheat bran (0.317 ppm) and fish meal (0.103 ppm) than in other ingredients of the animal diet (0.004-0.027 ppm) .

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Experiments were performed on species difference and diurnal variations in serum thyroxine (T₄) and T₃-binding capacity (TBC) in cynomolgus monkeys, beagle dogs, albino rabbits, and Sprague-Dawley rats. According to the competitive protein binding analysis, serum T₄levels of rats and monkeys were higher than those of rabbits and dogs, while monkeys showed a higher TBC than the other species. No sex differences were noticeable in dogs and rats. As to diurnal variations, dogs exhibited higher T₄level and lower TBC during the night, while no marked fluctuations were observed in those values with rats.

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Anamnestic serology was applied to checking infection of mouse hepatitis virus (MHV) in breeding colonies, revealing that, in a highly infected colony, animals of age 6 weeks or more had detectable complement fixing (CF) antibody. Mice of ages from 3 to 8 weeks from the infected colony showed higher resistance to challenge infection than those of corresponding ages from a non-infected colony, and difference was most evident at 8 weeks of age. CF antibody was detected 10 days after challenge in survivors from the infected colony challenged at 6 and 8 weeks of age but not in those challenged at 3 and 4 weeks of age. When dams from the infected colony had received repeatedly inactivated MHV, sucklings became to have antibody of a level practically equivalent to that of their mother, while the level lowered markedly towards 4 weeks of age. After challenge infection at 2 to 8 weeks of age those offspring from treated dams showed a strong resistance, but CF antibody was not detectable in most survivors challenged at 4 weeks or more. On the contrary, survivors from non-treated dams challenged at 8 weeks of age mostly had CF antibody. From these results, it is considered that a low level of maternal antibodies having been transmitted from dams play an important role for protecting young mice from infection with MHV and that higher resistance can be induced by natural infection at 6 weeks of age or later when antibodies of maternal origin has declined.

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