1) The growth of Candida albicans is inhibited, besides by B. coli, in the presence of other intestinal flora such as Staphylococcus aureus, Streptococcus, Pneumococcus, Proteus vulgaris and Pn eumobacillus. 2) The metabolic end products of Staphylococcus aureus show almost no harmful effects on the growth of Candida albicans.
3) When the growth of fresh strain of Candida albicans is compared in the peptone medium with that of the stale, the growth rate of the fresh is about 10 times of that of stale in 48?hour culture. Generally speaking, the symbiosis of B. coli and other intestinal flora with Candida albicans seems to be sustained within the limit of a certain balance of existence, which may be broken on the administration of antibiotics by the diminution or elimination of some of the sensitive organisms. In such a case, the energy source, mostly glucose; normally consumed by B. coli and other intestina flora will remain unused and be utilized by Candiiic albicans causing its excessive growth.

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1)In synthetic medium adde d with riboflavin, pyridoxin, folic acid or biotin, the development ofresistance was more promoted than in vitaminmedium.
2) Whereas the growth of resistant mutants was delayed than that of parent strains in vitamin-free medium, resistat mutants were equally or more promoted the growth than parent stains, when one of vitamins was added.
3) Those vitami ns seem to have some growth promoting factor to streptomycin resistants of E. coli.

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1)For the thiobarbituric acid test, a test solution containing free or acetylated sulfadiazine was diluted to the optimum concentration, 0.5 to 8. 0 mg per 100 ml, and adjusted to the optimum pH, about 1. 5, with I N hydrochloric acid buffer solution and a thiobarbituric acid solution. It is then heated in a boiling water bath for at least an hour, cooled at room temperature and its volume corrected. After centrifugation and between 30 and 60 mniutes after heating, calorimetric measurements of the solution were made with a photoelectric colorimter, using the 530 filter. The minimum concentation for accurate measurements was about 0.02 mg per 100 ml.
2) In the clinical blood sam ples, sera were used us testing materials and the proteins were precipitated with the same volumes of 15% trichloracetic acid.
3) In the clinical urine samples, urobilin, urobilinogen, bilirubin and acetone would formate color with thiobarbituric acid, but the normal urine, even in the presence of oxydation of pyridine group, did not interfere with the color imetric measurements.
4) Th e total blood concentration of sulfadiazine orally administered in combination with sulfamerazinc, isoxazine or marbadal showed certain patterns of fluctuation. These patterns were probably related to the difference in solubilities between sulfadiazine and the other component. The greater. the difference in solubilities, the greater was its effect upon the absorption of sulfadia zine. So, the mutual effect on absorption and excretion of orally administered sulfonamide mixture could best be observed in oral administration of sulfadiazine with isoxazine because of their greater solubility difference.
5) The blood level of sulfadiazine administered with isoxazine might take longer but not shorter, to reach its maximum than when administered alone. Several types of blood levels of sulfadiazine are produced according to the time required to reach its maximum blood level and the total amount absorbed.
6) Isoxazine, which is more soluble and more readily absorbed than sulfadiazine, showed no significant changes on combined administration with sulfadiazine in the time required to reach its maximum blood level, but coinciding with the maximum blood level of sulfadiazine, it showed a definite in its blood concentration and it remained lower than when administered alone.
7) In excretion, no significant differenc e could be found whether administered alone or in combination.
8) Desirable combination of sulfonamides for clinical application were discussed, based on the foregoing findings.

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Since it is plausible that the nucleotic-acid metabolism may be affected by bile, especially bileacid salt consisting of main component in it be assumed to play its principal role, it appears suggestive that the gene in bacterial cell may be inflicted with a variation. As the mechani sms in regard to the acquirement of durg-resistance, on the other, are, according to recent investigation, to be closely indivisible to the nueleotic-acid metabolism through their way to resistant aquirement, so some form of variant genes are inevitablely induced. In order to make these quesetionable points clear, the infuences of bile and its fraction to the resistant Staphylococcus aureus and Pneumococcus produced by antiobiotics are experimentally studied in vitro, and following results were obtained. 1) The resistance of Staphylococcus aureus and Pneumococcus to penicillin are inhibited to so me extent by bile. 2) In fractions of bile, bile-salt, especially desoxy?cholic acid Na, and taurocholic acid, are most influential on the resistance of bacilli. 3) There has been no influence On the resistant Staphylococcus aureus and Escherichia colt to streptomycin. 4) Also no influence is to be found in resistance of tubercle bacilli to streptomycin a nd INAH and back-mutation of them. 5) Bile makes the highly resistant Staphylococcus aureus sensitive to antibiotics to some extent, while not to other bacilli. 6) The Staphylococcus aureus and Pneumococcus pre-treated with bile differs from their original strains in behaviors to resistance, the for mer be reversible, while the latter inreversible.

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In order to study the influ ences of various antibiotics and antifungal drugs upon the metabolism of C. aibicans, I have investigated their influences upon the adaptive enzymes of the cells. Using a living cell suspension of C. alb. (F. D. A. No. 1001) as an enzymic preparation which cultured on Sabouraud-glucose agar media at 37. 5 °C for about 24 hours, I have studied the influen ces of various drugs (final concentration 1-10 mcgfcc) upon adaptive oxidation of substrates by using manometric technique of WARBURG. 1. Mannose and galactose are adaptively oxidized by C. alb.
2., Both the respiration and the adaptive oxidation of mannose and galactose are inhibited by 8-hydroxyquinoline. merzonin. 2-methy1-3-merca pto1: 4 -naphthoquinone, aureot hricin, candimycin, eurocidin and trichomycin, but not affected by penicillin G, chlortetracycline, oxytetracycline, chloramphenicol, dihydrostreptom ycin, propylparaben, so called “Dehyroacetic acid” and natrium azide.
3. In the case of using mannose or galactose adapted cells, the oxidation of mannose or galact ose is inhibited by 8-hydroxquinoline, m erzonin, 2-methyl-3-mercapto-1: 4-naphthoquinon e, aureothricin and candimycin, but not affected b y eurocidin and trichomycin. Namely eurocidin a nd trichomycin inhibit the formation of the ad aptive enzymes.

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