The action of adrenaline and noradrenaline on the heart and peripheral circulation in man has been studied (Goldenberg, Pines, Baldwin, Greene & Roh, 1948; Barcroft & Konzett, 1949), but their effects on the hepaticG circulation are uncertain. Bradley (1946), using the hepatic vein catheterization technique, described, in a preliminary communication, an increase in hepatic blood flow with adrenaline. Grayson & Swan (1950) used changes in the temperature of the human colon as a qualitative index of blood flow and noted colonic vasoconstriction with both adrenaline and noradrenaline.In the present study not only have the effects of adrenaline and noradrenaline on the hepatic blood flow been determined but also simultaneous changes in splanchnic carbohydrate metabolism. METHODSThe twenty-two subjects studied had no known hepatic dysfunction and were rested in bed and without food for 12 hr. Sodium amytal 0-2 g. was given by mouth 30 min. before the observations began.A , 1945). Twenty minutes after the infusion had begun blood samples were taken from the hepatic vein catheter and through an indwelling needle in an antecubital vein. At the same time 0-2 ml. capillary blood was withdrawn from the ear. The level of B.S.P. in the peripheral venous blood ws. estimated to ensure that it was greater than 1-0 mg./100 ml. plasma; two further sets of control samples were taken at 10 min. intervals. Adrenaline or noradrenaline were then added to the B.5.P. infusion so that the subject received the test substance at a constant rate for 30 tnin.* Lund Fellow of the Diabetic Association.

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Summary A genetical analysis has been carried out on thirty‐two patients with Wilson's disease from thirty families obtained largely from the New York area. Fourteen of the thirty‐two patients (43.75 %) were of eastern European origin (Jews) and eight (25.0 %) came from the Mediterranean (non‐Jews); both groups came from geographically circumscribed areas. A number of differences were observed between the patients who were Jews from eastern Europe and the Mediterranean and other groups. The Jews, on an average, tended to have more consanguinity, a later onset of the disease and, consequently, a relatively increased fertility. Clinically there was no predilection for either group to have a particular type of the disease. The Jewish group of patients had an increased variance in the serum copper and ceruloplasmin levels relative to the Mediterranean group. The patients with a normal level of ceruloplasmin came from the eastern Jewish group. Not all these differences were significant statistically and collection of more cases will be needed before firm conclusions can be drawn. The possibility that the eastern European Jewish population may possess a modifying gene and the possibility that more than one allele is present at the Wilson's disease locus is discussed. It should be emphasized that the evidence available is insufficient to state that ceruloplasmin is the primary gene product in Wilson's disease. If further evidence lends support to this view it will be necessary to perform structural studies on ceruloplasmin obtained from patients with Wilson's disease of various geographic origins in order to investigate the possibility of chemical allelism. This manuscript was written during the tenure of the position of Honorary Research Assistant at the Galton Laboratory, London. I am very much indebted to Prof. L. S. Penrose for his constant advice and for his critical reading of the manuscript.

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Recent population studies by starch gel electrophoresis have revealed an elaborate genetically determined polymorphism of human and primate transferrin, the iron-binding protein in serum. At the present time twelve different molecular species of human transferrin have been identified (1). Transferrins whose electrophoretic mobilities are faster than the common type C are labeled B, and slower moving variants are labeled D. With the exception of transferrin C, which is found in high frequency in all populations, particular variants are rare and appear to be restricted to particular populations. Thus transferrin B0-1 is found in Navajo Indians, B, in Caucasians, Dchi in Chinese, and D1 in Negroes. The gene frequency for each of these variants is approximately 0.05; the remaining seven variants have been reported only in isolated individuals.The glycoprotein nature of transferrin has been investigated by Schultze et al. (2), who found a 5 per cent carbohydrate fraction composed of hexose, hexosamine, sialic acid, and fucose. Schultze and Schwick (3) had earlier described a reduction in the electrophorefic mobility of transferrin after incubation with neuraminidase, a bacterial and viral enzyme which cleaves the glycosidic bond joining sialic acid to a protein molecule. A similar effect had been observed by Perlmarm, Tamm, and Horsfall (4) for urinary mucoprotein after incubation with influenza virus.A brief report (5) previously described the stepwise action of neuraminidase in removing the four sialic acid residues from the transferrin molecule. The present study is concerned with an extension of the neuraminidase effect from transferrin C to certain genetic variants of human and primate transferrin. In addition, the transferrins of cord blood and cerebrospinal fluid are shown to be related by the neuraminidase effect to adult serum transferrin. Amino acid analyses of three human transferrins and a primate transferrin are also given.