In 1940 Woods and Fildes (1) showed that p-aminobenzoic acid was able to inhibit the action of sulfanilamide on the growth of haemolytic streptococci in vitro. Since then the anti-sulfonamide activity of p-aminobenzoic acid was demonstrated in several species of bacteria both in vitro and in the animal body. For instance, Selbie (2) showed that p-aminobenzoic acid, administered by mouth, could inhibit the curative action, of sulfanilamide in experimental infections of mice with group A haemolytic streptococci. Findlay (3) confirmed the same inhibitory action following both intracerebral and intraperitoneal inoculation of haemolytic streptococci in mice. Rubbo and Gillespie (4) showed that p-aminobenzoic acid inhibited the bacteriostatic action of sulfanilamide on Clostridium acetobutylicum. Landy and Wyeno (5) reported experiments which demonstrated that p-aminobenzoic acid was capable of inhibiting the effect of sulfonamide drugs on the growth of streptococci, pneumococci and staphylococci in vitro. Strauss, Dingle and Finland (6) showed that p-aminobenzoic acid inhibited the anti-bacterial activity of sulfathiazole on pneumococci. McCarty (7) reported that p-aminobenzoic acid (given subcutaneously) was found capable of nullifying the curative effect of sulfapyridine (given peros) for type I pneumococcus infection in mice. Kimming (8) showed that the effect of sulfonamide compounds on gonococci in vitro was reversed by p-aminobenzoic acid. Kuhn, Möller and Wend (9) showed that p-aminobenzoic acid could interfere with the bacteriostatic action of sulfonamide compounds on streptobacterium plantarum.
On the other hand, in the case of the sulfonamide-sensitive viruses, Findlay (3) showed for the first time that p-aminobenzoic acid could inhibit the chemotherapeutic action of sulfanilamide on the virus of lymphogranuloma veiereum injected intracerebrally in mice. It appeared to be of interest to determine whether the chemotherapeutic action of the sulfonamide group of drugs on this virus was also inhibited in ti. vitro growth tests by p-aminobenzoic acid.
In viruses and rickettsiae, however, in vitro growth tests can be undertaken only by means of tissue culture method. In former studies (10) we showed that the virus of lymphogranulomaa venereum and typhus rickettsiae could be grown in deep columns of Maitland medium and their growth could be examined easily under microscope. Therefore, in the present study, the method of cultivation in deep columns of Maitland medium was used to test the actions of sulfonamide compounds and p-aminobenzoic acid on the virus of lymphogranuloma inguinale and typhus rickettsiae in vitro.
In the present paper the inhibition by p-aminobenzoic acid of the chemotherapeutic activity of sulfonamide drugs on the virus of lymphogranuloma inguinale in vitro is described. Furthermore, it is shown that p-aminobenzoic acid inhibits the growth of typhus rickettsiae in vitro, while sulfonamide compounds have no inhibiting effect on the growth of rickettsiae.

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Streptothricin is a well-known antibiotic found by Waksman and his collaborators (1) . However, there are more than two kinds of antibiotic substances which are very similar to streptothricin. Lavendulin and actinorubin reported by Kelner and Morton (2) are very resembling to Streptothricin. E. coli whose resistance to streptothricin has been forcedly raised becomes simultaneously more resistant to lavendul in and actinorub in than the normal culture. Umezawa and his collaborators (3, 4) found that antibiotic substances resembling to streptothricin were produced by various kinds of streptomyces, and called them streptothricin-group-substances.
Streptothricin-group-substances have the following characters. (1) They are produced by strains belonging to streptomyces. (2) They are adsorbed by activated carbon from their neutral solution and eluted into acid methanol. (3) A streptothricin-fast E. coli is more resistant to them than the normal culture. A streptomycin-fast E. coli is almost as susceptible to them as the normal culture. In this character streptothricin-group substances can be easily differentiated from streptomycin.
Ten strains of S. lavendulae, two strains of S. albus, one strain of S. ruber, one strain resembling to S. antibioticus, and five strains of S. fradiae, which all had been isolated by Umezawa and his collaborators (5, 6) were found to produce streptothricin-group-substances. Moveover, during testing the resistances of B. subtilis (N. R. R. L. B-558) and B. anthracis, it was found that antibiotic substances of all strains except the strains of S. fradiae showed a longer inhibition length against B. subtilis than against B. anthracis, but the antibiotic substance of S. fradiae showed a longer inhibition length against B. anthracis than B. subtilis. The antibiotic substance of S. fradiae seemed to be different from other streptothricin-group-substances.
In further studies the antibiotic substance of S. fradiae was found to be different from other streptothricin-group-substances in the antibacterial spectrum and the toxicity. The later appearing toxicity which was specific. for streptothricin was not found in the case of the antibotic of S. fradiae. And we decided to call the antibiotic of S. fradiae Streptothricin B, and the others streptothricin A, for among the streptothricin-group-substances streptothricin, the antibiotic of S. lavendulae, was first discovered.
Now the streptothricin A indicates the streptothricin-group-substances produced by various kinds of streptomyces other than S. fradiae. Whether the streptothricin. A is only one kind of substance or there are more than two kinds of streptothricin A, is not yet determined. Though streptothricin A was produced by various kinds of streptomyces, the later appearing toxicity was always observed. The later appear ing toxicity seems to be common to streptothricin A.
In the present paper the differences of streptothricin A and strepto thricin B are described.

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Chloromycetin was at first isolated by Bartz (1), Smith and others (2), Ehrlich and others (3) and soon afterwards also by us (4) . Bartz reported also the results of elemental analysis of chloromycetin, but now we could decide its molecular formula. In this paper the results of elemental analysis, determination of molecular weight, and testing the bacteriostatic effect by agar streak method are described.

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In 1924 H. Miura (1) isolated 2 strains of luminous bacteria from dead fish. He found that one strain decomposed glucose, maltose, dextrin, galactose, fructose, glycerol and mannitol and could not decompose sucrose, lactose and inuline, but the other strain decomposed only glucose, galactose, fructose and glycerol. In 1932 F. Fuhrmann (2) studied the influence of sugars on luminescence, and obtained the following results: Glucose, fructose and galactose did not increase materially the luminescence; and greater amounts of these hexoses produced acids and consequently inhibited luminescence. Cane sugar was without any material influence on M luminescence, while lactose in moderate amounts increased luminescence, but larger amounts inhibited it. In 1935 F. H. Johnson (3) studied the decomposition of carbohydrates, and polyhydric alcohol by luminous bacteria. He concluded that it was difficult to find any important correlations between the molecular configuration of the substrate and the ability of the organism to oxidize it, and only those compounds hawing 3 or 6 carbons were utilized. In 1942 M. Doudoroff (4) studied the anaerobic metabolism of facultatively anaerobic species of luminous bacteria. He observed that a few spesies of Photobacterium and Achromobacter harveyi decomposed glucose and produced chiefly formic acid, acetic acid, lactic acid, ethylalcohol, succinic acid and CO₂, while Photobacterium phosphoreum produced hydrogen and occasionally 2, 3-butvlene glycol.
The author studied the influence of carbohydrates and polyhydrin alcohol, obtained in hard conditions of post-war time, on growth and luminescence of luminous bacterium “Jidai No. 23”.

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It is now generally agreed that pyruvic acid holds a keyposition in the intermediary metabolism of carbohydrate, participating in both the anaerobic and aerobic cycles. Lactic acid is derived by reduction of pyruvic acid, and its complete oxidation requires oxygen and diphosphothiamine. In severee strenuous exercise, these metabolites accumulate in blood in a paralell manner, namely pyruvic acid shows the similar trend as does lactic acid (1) .
In the previous paper (2) we presented data showing that moderate exercise, which was continued for a fairly long time, had little effect on the levels on the acids, but both acids were increased markedly after strenuous exercise. In this paper, we shall present the more precisely followed curves of pyruvic and lactic acid concentrations of the blood after muscular activities of various grade.

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