663

Miller 5 has reported the same types of abnormality inthe foetuses of prediabetic mothers, before they had anyhyperglycsemia. Another suggestion is that the mother’shormones stimulate the infant both to grow abnormallylarge and to have islet-cell hyperplasia.1 .

Experimental work has yielded some clues to themechanism. Thus Hultquist’s 6 diabetic rats producedoversized young with a high incidence of islet-cell hyper-plasia ; but the increased weight of such foetuses was notassociated with an increase in body-fat, such as mighthave been expected if an excess of sugar and insulinwere responsible. Such fcetal oversize may be partlydue to prolongation of pregnancy, (which is presumablydetermined by changes in the hormonal milieu of thediabetic mother 7), but this cannot be the only cause.There is some experimental evidence that pregnancyimproves the diabetes of the mother,6 8 although in manthis is unusual.3 It has been supposed that foetal insulinreaches the maternal circulation and helps to compensatefor the mother’s insulin deficiency 2 ; but there is no

good reason for believing that insulin can cross the

placental barrier. The final assumption of earlier workerswas that at birth the foetus suddenly lost the source of itsextra sugar and was therefore left in a state of functionalhyperinsulinism which might terminate in fatal hypo-glycaemia. It is now appreciated, however, that theneonatal blood-sugar level varies considerably and maybe much lower than that of the adult, but that at thisage the body is relatively insensitive to the effects ofhypoglycaemia.9 10 Doubt has been expressed as towhether hypoglycsemia is especially likely in the infantsof diabetic mothers 10 11; and even if it were, the causewould not necessarily be hyperinsulinism. Perhaps whentests for plasma-insulin have been further refined, thesemay help to solve the problem.

5. Miller, H. C. Amer. J. med. Sci. 1945, 209, 447.6. Hultquist, G. T. Acta path. microbiol. scand. 1950, 327, 695.7. Snyder, F. F. Bull. Johns Hopk. Hosp. 1934, 54, 1.8. Carlson, A. J., Orr, J. S., Jones, W. S. J. biol. Chem. 1914, 17, 19.9. Pedersen, J. Blood Sugar of Newborn Infants during Fasting

and Glucose Administration. Copenhagen, 1952.10. Komrower, G. M. Arch. Dis. Childh. 1954, 29, 28.11. Potter, E. L. Pathology of the Fetus and the Newborn. Chicago,

1952; p. 343.

SIR ANDREW DAVIDSON’S RETIREMENTAT the end of this- month Sir Andrew Davidson leaves

the post in which he has done so much sound work andmade so many friends. Appointed chief medical officerof the Department of Health for Scotland in 1941, hewas a graduate of the public-health service, in whichhe had served successively in Glasgow, Surrey, and theNorth Riding of Yorkshire. He had both the right kindof experience and the right mental equipment for adoctor-administrator : whatever he felt he had to do, orwhatever he undertook to do, he did with all his might.Taking office early in the war, he was preoccupied

with the casualty side of Civil Defence and with theconduct of the several emergency hospitals which werebuilt in Scotland and are now incorporated in the NationalHealth Service. At that time, Mr. Thomas Johnstonwas Secretary of State for Scotland, and he and Davidsonformed a remarkably energetic team, with drive and

imagination. For instance, the Clyde Valley experimentfor restoring the health of workers on the verge of break-down, and the scheme for reabling disabled miners,attracted attention by their originality of conceptionand execution. After the war his attention was -concen-trated on preparation for the National Health Service,and on its introduction. The N.H.S. in Scotland, operatingunder a separate Act of Parliament, is substantiallydifferent from the English model, and it came intooperation with surprising ease. For this, Davidsondeserves part of the credit ; but what was more remark-able, ina man grappling with so many complexitiesand difficulties, was that he never mistook the newservice for an end in itself, regarding it always as a

means of improving the health of the people whom heknew so well.

Though so deeply immersed in policy and administra-tion, Davidson found time to expound his ideas of futureprogress, and of the underlying purpose of a nationalhealth programme, which were set forth in lectures andpapers chiefly published in America. Last year, withsome reluctance after a lengthy illness, he undertook aseries of addresses at universities in the United Statesand Canada. Similarly in the affairs of the WorldHealth Organisation he has regularly played a helpfulpart. Indeed abroad as well as at home he has wonthe kind of reputation that goes only to those who com-bine idealism with humour and a strong mind with awarm heart. We trust that rin retiring, by his owndecision, from the service of his department he will notalso retire from the service of Medicine.

1. McMaster, P. D., Hudack, S. S. J. exp. Med. 1935, 61, 783.2. Burnet, F. M., Lush, D. Aust. J. exp. Biol. 1938, 16, 261.3. Enrich, W. E., Harris, T. N. J. exp. Med. 1942, 76, 335.4. Dougherty, T., Chase, J., White, A. Proc. Soc. exp. Biol., N.Y.

1944, 57, 295.5. Oakley, C. L., Warrack, G.H., Batty, D. J. Path. Bact: 1949,

61, 179. 6. Harris, T. N., Grimm, E., Mertens, E., Ehrich, W. E. J. exp.

Med: 1945, 81, 73.7. Fagraeus, A. J. Immunol. 1948, 58, 1. 8. Chase, M. W. Fed. Proc. 1951, 10, 404.9. Harris, S., Harris, T. N., Farber, M. B. J. Immunol. 1954, 72,

148, 161.

ANTIBODY TRANSFER

THERE is little precise information about the site andthe mechanism of antibody formation. In the case ofbacterial cells and viruses and some other antigens, thespecific antibodies are elaborated in regional lymph-nodes,1—5—by lymphocytes according to most Americanworkers, by plasma-cells according to Scandinavianworkers. 7

Transplantation of tissues from an immunised animalconveys to the new host the power to produce antibodies,and cells from the spleen or lymph-nodes of sensitisedguineapigs give rise to sensitisation in animals to whichthe cells are transferred. 8 After bacterial cells andviruses had been injected into the hind-foot pad of arabbit the popliteal lymph-node was excised and thelymphocytic cells were isolated, washed, and injectedintravenously into normal rabbits. Specific antibodiesto the bacterial cells and viruses appeared in the blood-stream of the rabbits which had received the injectionof lymphocytes. Apparently this was not explained bythe passive transfer of antibodies from the donor rabbit,nor was any detectable amount of antigen transferred.9 9Possibly antibody precursor was present in the trans-ferred cells and the conversion of this to antibody wascompleted in the recipient rabbit: It seems more likely,however, that the transferred cells had been " educated "to produce specific antibodies and they continued to doso even when transferred from the immunised rabbit tothe new host.

Cells from the regional popliteal lymph-node weremore effective than spleen cells in conveying antibodyformation. When the cells were damaged by freezing orheat, ultraviolet irradiation, or lysis they no longerproduced antibodies in the recipient animal ; but

repeated washing had no effect on this function. Aftercortisone had been administered to the donor rabbitsthe lymph-nodes contained fewer cells ; but the cells

present produced antibody no less effectively than thosefrom untreated animals. Cells obtained from animalsfour days after immunisation were as effective whentransferred to cortisone-treated animals as in normalanimals, but cells transferred only two days afterimmunisation were sometimes less effective in thecortisone-treated recipients. This suggests that the

antibody-forming mechanism was incomplete two daysafter immunisation and that the cortisone interferedwith its development.