We measured creatine kinase (CK, EC 2.7.3.2), CK-MB isoenzyme activity and mass concentration, and distribution of CK isoenzymes (by electrophoresis) in serum from five members of one family. The mother and two young children showed CK-IgG complexes in their sera. The concentration of the CK-IgG complexes in the children decreased over time, suggesting that the complex involved maternal IgG and had been transferred across the placenta from the mother to her children.

Glycyrrhetinic acid was found to resemble the Δ4‐3‐ketosteroids in antagonising uterine growth response to exogenous oestrogen in doses which did not interfere with somatic growth or the oestrogenic effect on pituitary trophic hormones. The anti‐oestrogenic effect was not mediated through gonadal inhibition, adrenal stimulation or potentiation of endogenous adrenal corticoids. Glycyrrhetinic acid is neither androgenic, oestrogenic nor anti‐androgenic. However, it does resemble the glucocorticoids in depressing granuloma tissue formation in adrenalectomised rats.

The desexycorticosterone-mimetic action of ammoniated glycyrrhizin on electrolyte and water metabolism and on pituitary-adrenal function, was demonstrated in rats. Retention of sodium and water was observed in both intact and adrenalectomized rats during 4 hour minerosteroid assays, the degree of retention being a function of log dose. In intact rats, the antidiuretic effect of glycyrrhizin was immediate and cumulative, while retention of sodium appeared only after a latent period and did not increase with time. Adrenalectomized rats, 3 days after the operation, showed a more marked antidiuretic effect than intact rats, but no greater retention of sodium. Rats receiving glycyrrhizin prior to histamine stress showed a marked decrease in adrenal ascorbic acid depletion, suggesting that glycyrrhizin had suppressed the output of ACTH. Whether glycyrrhizin acts on the same target organ as desoxycorticosterone in producing sodium and water retention is still an open question. However, the fact that it is capable of producing a pituitary-adrenal inhibition which resembles that of naturally occurring adrenal steroids is further evidence of the strong pharmacological resemblance between glycyrrhizin and desoxycorticosterone.

The adrenal ascorbic acid depletion parameter was used to determine the pituitary-adrenal response to acute stress, the adrenal responsiveness to exogenous corticotrophin (ACTH), and the pituitary ACTH reserve in alloxan diabetes. The pituitary-adrenal response to histamine (0.5 mg/100 g i. p.) 1 hour before sacrifice was significantly impaired in uncontrolled diabetes. Elimination of glycosuria by insulin administration (7 days) restored the response to normal though adrenal hyperplasia was still evident. The impaired stress response was not due to a decrease in the adrenal responsiveness or the pituitary ACTH reserve. The adrenal ascorbic acid depletion response to exogenous ACTH (measured against saline controls) was normal. Pituitary extracts of diabetic animals produced the same degree of adrenal ascorbic acid depletion in hypophysectomized animals as pituitary extracts of normal animals. The adrenal hyperactivity previously reported to exist in uncontrolled diabetes is accompanied by a decreased ability to release preformed ACTH in response to acute stress. The metabolic stress of diabetes resembles other chronic stressors which impair the secretory mechanism at the hypothalamo-hypophyseal level.