I studied the sterilizing action of dibasic fatty acids C_nH_2n•(Co₂H)₂ on putrifactive bacteria, Bac. typhosus and Vib. cholerae, and also compared the sterilizing action between dibasic and monobasic fatty acids.
Results are as follows:
(1) At the same molecular concentration, oxalic acid (C₂) is the stron-gest, malonic acid (C₃) is the next, and from malonic acid the sterilizing power suddenly greatly diminishes. From C₆ acid the sterilizing action of acids gradually increases, according to the increase of the number of C atom.
(2) Anions of C₂ to C₆, acids have no sterilizing action. According to the increase of the number of C atom from C₆ acid the sterilizing power of anions gradually increases, but its action is very weak.
(3) Among salts of Na, Ca and N₄, Ca salts have a somewhat weak sterilizing power, and NH₄, salts have a somewhat long surviving period for bacteria.
(4) At the same molecular concentration of acids having the same number of C atom, from C₂ to C₃ acids, dibasic fatty acid is the strongest, unsaturated monobasic fatty acid is the next, and saturated monobasic fatty acid is the weakest. The fact is chiefly due to pH. From C₅ acid, accor-ding to the increase of the number of C atom, the sterilizing action of niono-basic fatty acids are stronger than those of dibasic fatty acids. The fact due to the effect of undissociated molecules of each acids.
(5) At the same pH, sterilizing action of saturated monobasic fatty acid is the strongest, unsaturated monobasic fatty acid is the next and didasic fatty acid is the weakest of all. The fact is due to the difference of mole-cular concentration of each acids.
(6) There is no special relation between the number of CO₂H group and the strength of sterilizing action.

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(1) The glycogen contents in the liver of pigeons, and albino rats suffering from vitamin B₁-deficiency were estimated.
(2) In the case of pigeons, those which developed the disease without loosing much in body weight stored up more glycogen. than the normal ones, i. e. 1.5 to 2.0 times higher than the latter, while those suffered from severe inanition and consequently heavily loss in body weight had always less glycogen than the control. In pigeons cured by the administration of active oryzanin (B₁-preparation), the liver glycogen was nearly normal.
(3) The underfed birds had always less glycogen than the normal ones.
(4) In albino rats fed on carbohydrate rich synthetic diet and developed the disease, the liver glycogen was without exception 1.5 times higher than the normal ones. In the animals cured by active oryzanin, the glycogen content was again reduced to the normal level.
(5) Though the rats fed on B₁-free, high-fat diet lacking carbohydrates have shown the typical symptom of avitaminosis, yet there was no increase of glycogen in the liver.
(6) It may be assumed that the abnormal increase of glycogen in the liver of avitaminous animals fed on B₁-free diet is a secondary phenomenon of the disease, but not the cause of it.
(7) As the diets used in these experiments contained B₂ in the form of autoclaved yeast, it can be concluded that B₁ has played an important rôle for the metabolism of liver glycogen.

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