ARACHIDONIc acid is widely distributed in the animal body and its presence has been shown to be essential for the maintenance of the normal health of the rat. In rats which have suffered for many months from the fat deficiency disease first described by Burr & Burr [1930] the liver was found to be entirely free from this acid and only very small amounts were detected in other parts of the body. It was, however, retained if linoleic or arachidonic acid itself was included in the diet of the rats. The conclusion was drawn by Nunn & Smedley-MacLean [1938] that the rat can probably synthesize arachidonic acid using linoleic acid as its starting material. At this time all that was known as to the structure of arachidonic acid was that it contained a normal chain of 20 carbon atoms since it yielded arachidic acid on reduction [Bosworth & Sissons, 1934], that four double bonds were present and that, from the normal iodine value, these were unconjugated. We were therefore anxious to determine the position of the double bonds in the chain and to compare the structure of this acid with those of linoleic acid.Shinowara & Brown [1940] have, however, recentlypublished some preliminary results on the structure of this acid and suggested a formula though they emphasize that it is only tentative. The determination of the diene number of methyl arachidonate is interpreted by these authors as indicating the presence of about 5 % of conjugated bonds derived either from the presence of a small proportion of an isQmeric ester or from a rearrangement of the ester under the conditions of the diene determination. However, in the bulk of the acid examined, the bonds were not conjugated. The methods of oxidation used by these authors were ozonolysis and oxidation with permanganate in acetone solution. We, on the other hand, have used the action of an %queous alkaline permanganate solution and have arrived at entirely different conclusions from those drawn by Shinowara & Brown. We should have preferred to repeat and extend our experiments before publishing our results but in view of the communication of these authois and of the postponement of our experiments necessitated by present conditions, we have decided to publish them.Shinowara & Brown, with their methods of oxidation, did not detect any aldehyde higher than acetaldehyde, nor did they detect oxalic acid but they obtained indications of adipic and succinic acids and concluded that a double bond existed between the 18th and 19th carbon atoms and that the group : C. CH2 . C: characteristic of linoleic and linolenic acids was not present in the molecule.'We on the other hand deduce from our findings that the terminal chains of ten carbon atoms are similar in structure in both arachidonic and linoleic acids and that certainly three and almost certainly four of the groups CH. CH2. CH: occur in the arachidonic molecule.

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SUMMARYThe effect of antigens of Bordetella pertussis and their antibodies on brain infections by B. pertussis in mice are suppression of an infection immediately, so that the initial 90 % loss due to leakage from the brain is maintained or the numbers of bacteria are reduced even further, sometimes with complete sterilization particularly after a small lethal challenge of 10 LD 50 (mechanism 1), and a delayed antibacterial activity in vivo which does not begin until 3 days after challenge (mechanism 2). The first, immediate reaction is over in 2-3 days; the second is maintained from 3-4 days onwards, and results in elimination of the bacteria and protection of mice.The parts played in vivo in overcoming infection in these two ways by two antigens and their respective antibodies have been investigated. These antigens are a lipopolysaccharide capable of eliciting an antibody which is bactericidal in vitro in the presence of complement called the 'bactericidal antigen', and the mouse

SUMMARYWhen mice were injected intracerebrally with doses of Bordetella pertussis vaccine greater than 5 ImD 50 and challenged intracerebrally 14 days later with virulent B. pertussis there was an immediate reduction in the numbers of organisms.An analysis of this in vivo bactericidal effect has shown that large doses of an unrelated vaccine, Salmonella typhosa, equivalent in cell mass to about 50 ImD 50 of B. pertussis vaccine can achieve this effect, so for such doses the effect must be partly non-specific. This action is not maintained and so is not ultimately protective. Local immunoglobulin was also demonstrable 14 days after 300 ImD50 of B. pertussis vaccine but following smaller doses of 10-20 ImD 50 it could not be found until after the mice had been infected and the blood-brain barrier impaired.A similar immediate reduction in the numbers of infecting organisms inoculated 1 day after vaccination has been shown to follow very small, non-protective doses of vaccines unrelated to B. pertussis and to be achieved with lipopolysaccharide and endotoxin isolated from B. pertussis. Brains were not sterilized and only in mice receiving protective B. pertussis vaccine was the lowering of infection maintained beyond 2 days and the brains eventually sterilized.The antibody passively protecting mice against intracerebral infection was found in the 19 S and 1 1 S globulin fractions of the serum of once-vaccinated mice and in the 11 S and 7 S fractions of the serum of rabbits and ascitic fluid of mice receiving repeated doses of vaccine. The IgM probably eliminated infections by immediate sterilization but had to be present locally to do so since it was unable to pass from the circulation into the brain, and was therefore inactive when injected intraperitoneally. The IgA and IgG were not so restricted and both the 11 S and 7 S globulins were capable of exerting an immediate suppressive effect on infecting organisms. The 7 S globulin was also capable of a maintained or delayed suppressive effect.Lymphocytes from fully protected once-vaccinated mice, transferred 2-3 weeks after intraperitoneal vaccination, were able to confer some protection when injected intraperitoneally or intracerebrally into recipient mice infected 2 weeks after transfer. Homologous, non-concentrated antiserum from once-vaccinated

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