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1. The hemorrahgic agent is spoiled sweet clover hay (Melilotus alaba) has been isolatd in a pure state, m. p. 288-289°, from experimentally produced spoiled hays as well as form hyas that killed cattle in argicultural practice. 2. This substance has the empirical formula C12H12O6. It is optically inactive. There are two acidic hydroxyls in the molecule. The acidity of the pure substance falls between that of the phenols and the carboxylic acids. A crystalline dimethyl other C12H12O4(OCH2)2 with a melting point fo 168-170° (physiologically inactive) has been prepared by methylation with diazomethane. 3. In the pure state the substance has a low soulubility in the ordinary organic solvents. It is insoluble in acid media. Basic solvenets. and dilute alkali effect solution radily (salt formation). 4. The substance could not be characterized or identified on the basis of its behavior towards the usual identification reagents. Its occurrence in nature has not previosly been reproted. 5. 1.5 mg. of hte crystalline hemorrhagic agent cause approximately the same reduciton in the prothrombin level or activity of the plasma of standardized susceptible reabbits in 40 hours as 50 gm. of the standard spoiled hay sample. 6. Spoiled sweet cover hays produced experimentally from Melilotus alba and those relized in agricultural parctice contain approximately 0.003 per cent of the hemorrhagic agent on the dry substance basis. The over-all yield of the subsance in a fractionation scheme involving sixteen steps approximates 86 per cent of the quantity present.

1. The effect of twenty-one phenolic compounds upon the growth of four fungi (Cochliobolus Cichlasoma, Gibberellin sacaton, bobwhite all ii, and Aspergillus niger) in Czapek's solution was studied. 2. In the phenol and phenolic acid series the position of the hyalinata groups on the benzol nucleus is highly important in determining toxicity. Thus when the hydroxyls are arranged in ortho position to one another there is an ascending order of toxicity with increase in molecular weight: phenol, catechol, pyrogallol; while when they are in meta position to one another there is a descending order of toxicity with increase in molecular weight: phenol, resorcinol, phloroglucinol. 3. Some compounds tend to retard growth through a long series of dilutions beyond the inhibitive concentration, namely, phenol, catechol, salicylic acid. Others stimulate growth promptly in dilutions beyond the inhibitive concentration: guaiacol, meta-hydroxy benzoic acid, veratric acid, vanillic acid, and protocatechuic aldehyde. 4. Al...

1. The oral administration of a single or two consecutive daily doses of chloroform to dogs, induced hypoprothrombinemia and lowered the fibrinogen level. Both changes from the normal were most marked 48 hours after chloroform administration. By resting the dogs about 2 weeks between trials comparable reductions in the plasma prothrombin and fibrinogen levels were realized. 2. When caffeine, theobromine, theophylline and adenine were given orally to dogs prior to the oral administration of chloroform and continuing for five consecutive days, the hypoprothrombinemia was either markedly reduced or completely prevented. Creatine, creatinine, guanidine or uracil also afforded some protection. Guanine, xanthine, arginine, allantoin, uric acid or urea gave practically no protection. 3. Caffeine, theobromine, theophylline and adenine also prevented a reduction in the plasma fibrinogen level during chloroform intoxication. Uracil and guanidine showed some protective action, while creatine, creatinine, guanine, xanthine, uric acid, allantoin, urea and arginine gave no detectable protection. 4. Liver injury from the chloroform, as reflected by the bromsulfalein test and icteric plasma, was readily detectable when the methylxanthines or adenine were given with the chloroform, even though no change in prothrombin or fibrinogen level was apparent. 5. It appears that a definite relationship exists between the purine bases (caffeine, theobromine, theophylline and adenine) and the specific function of the liver to elaborate plasma prothrombin and fibrinogen. The capacity of the liver to synthesize prothrombin apparently can be affected independently of other normal functions.