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It is generally agreed that glucose is absorbed from the mammalian intestine by an active process, but the details of this are still not known with any certainty. It 10-20 mg/100 ml. higher than in the arterial blood when a solution of 13-5 % glucose was present in the intestine. With a concentration in the intestine 100 times that in the blood an enormous gradient for diffusion existed, and from such an experiment no conclusions could be drawn as to whether the glucose appearing in the mesenteric blood was actively or passively transported. Recently, Hestrin-Lerner & Shapiro (1953, 1954) claimed that glucose was absorbed in a form which was neither glucose nor lactic acid, but this claim could not be substantiated in experiments in vitro by Newey, Smyth & Whaler (1955). The present work deals with a quantitative investigation of the fate of glucose absorbed from the intestine in vivo, and with an attempt to determine in what form the absorbed glucose appears in the mesenteric blood.In preliminary experiments a solution to the problem was sought by chemical estimation of the glucose and lactic acid in the intestinal lumen and in the blood. The glucose disappearing from the intestine was measured, and at the same time the change in the glucose and lactic acid contents of the blood passing through the intestine was determined. These attempts proved unsuccessful because of the fluctuations not only of glucose but also of lactic acid in the arterial blood during the experiment. Other difficulties were the relatively large amounts of glucose brought to the intestine in the arterial 37-2

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SUMMARY Carrageenin pellets, implanted subcutaneously in adrenalectomized rats, produced in 5 days compact, easily dissected granulomata. Accepted anti-inflammatory steroids administered as single daily subcutaneous injections or in the diet, but not as single daily oral doses, reduced the granuloma wet weight. The relative anti-inflammatory activities of cortisol, prednisolone and betamethasone, administered subcutaneously or in the diet, duplicated their relative clinical values. The relative activity of dexamethasone to cortisol was three times that reported on patients. Corticosterone acetate was weakly active in this test, desoxycorticosterone acetate increased granuloma weight, and oestrone, mepyramine maleate, mersalyl, progesterone, norethandrolone, testosterone propionate and Pitressin were inactive.

Cortisol, prednisolone phosphate and the free alcohols and 21-phosphates of betamethasone and dexamethasone have been compared for thymolytic activity by the oral and subcutaneous routes in both sexes of two strains of rats and two strains of mice. The relative potency of betamethasone and dexamethasone differed with the route of administration and the sex, strain and species of animal employed. In female mice of the A2G strain, betamethasone was as potent as dexamethasone; in male mice of this strain, and in both sexes of GFF mice, WAG rats and PVG rats, betamethasone was much less potent than dexamethasone.