MIYA, MARCUS AND PHELPS 



production following cold exposure, the exact cause and effect 

 relationship remains obscure. 



At present we are investigating the possibility that the virus may 

 be present but inactive as a result of the acclimatization, but have 

 the potential to cause disease or death if the challenged animal is 

 removed from 2° C to 21° C, The situation could be analogous to that 

 observed by Sulkin et al. (1960) with regard to bat rabies virus. 



A brief discussion of the experiments with the mouse neoplasm is 

 in order. Goldfeder (1941) reported that the environmental tempera- 

 ture has a definite effect on the growth rate but not the viability of 

 sub cutaneous ly inoculated tumor cells. CXir results are similar in 

 this respect. Although a delay in mortality occurred, no significant 

 differences in the final mortality ratios were observed when mice 

 exposed to cold were comparedto mice challenged and kept at 21 C. 

 An obvious working hypothesis is that the lowered skin temperature 

 of mice kept at 2° C inhibited tumor cell metabolism until the tumor 

 cells became acclimatized to the lower temperature. Once this 

 occurred, it may be guessed, the growth rate of the acclimatized 

 tumor cells was the same as for the controls. 



The same temperature effect may be used to explain the delay in 

 mortality of mice inoculated intraperitoneally; that is, the core 

 temperature of 2^ C exposed mice is about 2° C higher than 

 mice kept at 21° C. This increased internal temperature may 

 either alter tumor cell metabolism or allow for selection of 

 tumor cells capable of growth at the new temperature. Work 

 is continuing on this aspect of low ambient temperature and 

 host resistance. 



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