fatty livers are rare, is additional supporting evidence that insulin-sensitive diabetes probably is of pancreatic origin, while insulin-insensitive diabetes is due at least in part to a pituitary factor. HYPERCALCEMIA, HYPOPHOSP~ATEMIA AND SALT Loss CAUSED BY THIOCYANATE. Richard Gubner, M.D., Brooklyn, N, Y. (From the Medical Department, Equitable Life Assurance Society of the United States, and the Dept. of Medicine, State University of New York College of Medicine.) Subjects with hypertension given thiocyanate even when blood levels are maintained below 12 mg. per cent not infrequently develop side reactions, notably sluggishness, muscular weakness and gastrointestinal symptoms. The present study suggests that these symptoms are due to hypercalcemia and hypophosphatemia associated with renal loss of electrolytes, i.e., phosphate, calcium and sodium chloride. In five of six subjects with normal renal function whose average thiocyanate blood level was 8.2 mg. per cent the Robinson-Power-Kepler test of urinary salt loss was abnormal. Adrenal function, as studied by the eosinophile response to epinephrine, was normal (average initial eosinophile count 177/mm3, average fall three hours after 0.5 mg. epinephrine, 57 per cent). There is no evidence therefore that thiocyanate produces adrenal insufficiency. Thiocyanate specifically inhibits carbonic anhydrase, which is responsible for renal tubular acidification of urine and conservation of sodium, and its effect in causing salt loss is probably due to inhibition of carbonic anhydrase, as is the case with sulfanilamide. In eight subjects receiving thiocyanate for periods varying from four weeks to eight years, with an average blood level of 8.15 mg. per cent, the serum calcium was uniformly elevated (average 13.2 mg. per cent, highest 15.2 mg. per cent), and the blood phosphorus was significantly lowered (average 2.8 mg. per cent, lowest 2.1 mg. per cent). The Sulkowitch test for urine calcium was highly positive in all these subjects. These electrolyte changes as well as the symptoms produced by thiocyanate resemble those occurring in hyperparathyroidism and it appears that the action of thiocyanate on the renal tubule is similar to that of the parathyroid hormone. Osteoporosis has been reported in subects receiving thiocyanate for sustained periods. It is suggested that the electrolyte changes produced by thiocyanate may have therapeutic application when it is desired to produce salt loss or to elevate blood calcium. EFFECT OF EXOGENOUS THYROID HORMONE ON THYROID FUNCTION OF NORMAL HuMAN SUBJECTS AS DETERMINED WITH RADIOACTIVE IODINE. Monte A. Greer, M.D., Boston, Mass, Although it has been known for many years that a reciprocal relationship appears to exist between the levels of circulating thyroid hormone and pituitary thyrotrophin, until recently a direct estimation of thyroid activity in man was not feasible. A study was made of the thyroid function of over thirty normal human subjects by following the rate of accumulation in the thyroid gland of an administered dose of radioactive iodine by means of serial counts with an externally placed shielded Geiger counter. Following control studies the subjects were given graded daily doses of desiccated thyroid and determinations of their thyroid activity were repeated at intervals of a few days to several months. The accumulation of 1131 by the thyroid glands of all subjects was suppressed within a few days by the administration of sufficient exogenous hormone to the levels seen in myxedema. The amount of U.S.P. desiccated thyroid required to produce this suppression varied from 60 to 180 mg. per day. This study is interpreted as demonstrating that the administration of physiologic amounts of exogenous thyroid to normal human subjects results in a decrease in the function of the subject’s own thyroid gland equivalent to the dosage of the exogenous thyroid administered. The subject will maintain a stable euthyroid level of circulating thyroxine unless toxic amounts of exogenous hormone are administered. STUDIES ON THE PRECIPITATION OF CEREBROSPINAL FLUID PROTEINS BY ZINC SULFATE. illfred M. Donovan, M.D., Joseph M. Foley, M.D. and William C. Moloney, M.D., Boston, Mass. (From the Clinical Research Laboratory of the First and Third Medical Services and the Neurological Unit, Boston City Hospital.) Abnormalities of protein fractions in the cerebrospinal fluid are known to occur in certain neurologic disorders but their demonstration in the routine clinical laboratory has been re-