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The racemic(14)C-and(3)H-labeled alpha and beta derivatives of octadecyl glycerol ether (batyl alcohol) and of hexadecyl glycerol ether (chimyl alcohol) of high specific activity were synthesized by treating the appropriate alkyl halides with a large excess of the potassium salts of isopropylidene or benzylidene glycerol. By use of the trifluoroacetic anhydride esterification procedure, the labeled diesters of alpha and beta octadecyl and hexadecyl glycerol ethers were prepared. The labeled monoesters of beta octadecyl and of beta hexadecyl glycerol ethers were isolated from the reaction mixtures by silicic acid column chromatography.

An agar plate test is presented as a screening test for phage induction capacity of various chemicals.

A guide or template is described which facilitates placing the cylinders on the agar surface in the plate assay of penicillin. The general plan of conducting the assay is discussed and several advantages of the use of the guide are noted. We wish to thank Mr. Albert G. Sterling, instrument maker, for fabricating the guide and the aluminum cylinders.

The metabolism of(14)C- and(3)H-labeled alkyl glyceryl ethers after intraperitoneal injections was examined in the liver and intestine of the rat. Additionally, in vitro experiments were conducted with intestinal homogenates and intetinal contents.From these investigations it was concluded that the liver and the intestine metabolize the alkyl glyceryl ethers very differently. Intestinal contents can alter alpha-batyl alcohol, as indicated by preliminary experiments, and intestinal cells contain enzyme systems which convert the alkyl glyceryl ethers to the mono- and di-acyl derivatives. Very little esterified glyceryl ethers were found in the liver lipids. The intestine contains an enzyme system which, although it has a greater specificity for chain length and for isomeric position of the ether than that of the liver system, does cleave the glyceryl ethers.From in vivo studies, of intestinal tissue it was concluded that all of the injected glyceryl ethers were converted intact the ethanolamine, serine, and choline alkyl glyceryl ether phospholipids; with the use of alpha-batyl alcohol, the phosphatidyl ethanolamine fraction, contained most of the labeled glyceryl ether phospholipid with beta-batyl alcohol, alpha-chimyl, and beta-chimyl alcohols, the phosphatidyl, choline fraction contained most of the labeled alkyl glyceryl ether phospholipid. No significant amount (<1%) of labeled alkyl glyceryl ether phospholipids was found in any of the rat-liver lipids.

Streptomycin held in solution in concentrations of 100 and 1,000 microg./ml. at 10 degrees C. is stable at pH 6.0, 7.0, and 8.0 for a period of three months. The depressor effect observed in the turbidimetric assay appears to be the result of two factors, buffer salt concentration and pH, and is most marked at pH 6.0. Almost normal activity reappears at pH 8.0 even in the presence of the greater concentration of phosphates.

Sulfonamide-resistant strains of Staphylococcus aureus produce greater amounts of p-aminobenzoic acid than do their parent strains. This synthesis occurs both in the absence and in the presence of sulfonamides. The quantity of p-aminobenzoic acid synthesized by resistant strains appears sufficient to account for their resistance to sulfonamide drugs. On the basis of this evidence, it is suggested that the development of ability to synthesize p-aminobenzoic acid in excess of the normal metabolic requirements, as a result of continued exposure to sulfonamides, explains the phenomenon of sulfonamide fastness in Staphylococcus aureus.