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ADRENALECTOMY, CHOLINE AND LIVER FAT 131 logous, phage-susceptible parent strain. A typical comparison of fibrinolysin production by parent strain and phage-resistant variant is recorded in Fig. 2. Within the limits of the experimental error the population changes in both flasks were identical throughout the tests so are not recorded in the figure.From Fig. 2 it is seen that while both flasks produced fibrinolysins at the same rate during the initial stages of population increase, the phage-susceptible parent strains rapidly destroyed or otherwise inactivated the fibrinolytic enzyme after reaching maximum titer. This destruction, however, did not take place (or was counterbalanced by continued fibrinolysin production) with the homologous 'phage-resistant variants, If as a result of local phage injections all local streptococci could be destroyed, bacteriophage therapy would presumably aid in preventing the spread of streptococcus infections. The danger of the local production of phage-resistant variants with heightened fibrinolytic function and presumably heightened virulence,2 however, would seem to contraindicate phage therapy in local streptococcus infections. This conclusion is in line with the experimental evidence reported by Bronfenbrenner and Sulkin' in their study of the local therapy in experimental staphylococcus infections in rabbits.

\Vhen rats are fasted they develop a ketonemia and frequently it is high enough to produce a measurable ketonuria. The height of the ketosis is determined by many factors. When the diet is low in choline and in protein the liver becomes fatty' and on subsequent fasting there is a very substantial ketonuria."! I t seemed probable that this was incident to the fatty liver. However, since we have been unable to obtain a good correlation between the degree of ketosis and the amount of fat in the liver we have examined the factors which determine the extent of the fasting ketosis in question.Deuel, ef ~l . ,~ have found that choline administered during the period of fasting does not appreciably affect the ketosis of fasting fatty liver rats. \Ye have confirmed this observation. Neither does the addition of choline to the diet prior to fasting, although it prevents the accunlulation of fat in the liver, influence the subsequent ketosis. The only possibility left is that the ketosis of fasting rats is determined by their protein intake prior to fasting. This has been demonstrated in diets containing variable concentrations of casein, all containing 0.5 % choline hydrochloride which insured livers low in fat when the fasting was commenced. The "0' protein diet was composed of sucrose 60, cod liver oil 2.5, Crisco 30, Standard Salt Mixture (Osborne and Mendel) 5, and Yeast Extract (Vitamin E Powder, The Harris Laboratories) 2. The other diets contained 5 , 15 and 30% of casein respectively at the expense of the sucrose. Each group consisted of 5 adult male rats with an average body weight of 324 g . They had been receiving the special diets for 10 days before fasting was commenced. The protein intake tabulated per rat per day is the average of the 10-day period of feeding.The data of a typical experiment recorded in Table I show very clearly the influence of the protein intake preceding a period of fasting upon the degree of fasting ketosis. Our ketonuria data as a ~ __ 1 Best, C. H., and Wilkinson, H., Biochem.

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