John F. Mueller

Pathologic Physiology of Mammalian Blood Platelet Utilizing P32 Tagged Rabbit Platelets.

Summary 1. Purified, unagglutinated platelet suspensions prepared from rabbit blood do incorporate radioactive phosphorus readily, and therefore lend themselves to life span studies in vivo. 2. These studies indicate that transfused rabbit radioactive platelets are rapidly removed from the peripheral blood and the radioactivity recovered in organs of the reticuloendothelial system, namely spleen, liver, lung and bone marrow. 3. The problem of viability of these platelets is discussed. The evidence suggests that damage has occurred during manipulation. 4. These observations are important primarily in demonstrating aspects of metabolism and destruction of platelets.

The effect of pyridoxine deficiency induced by desoxypyridoxine in human subjects upon the excretion of N1-methylnicotinamide after tryptophan administration☆

There is evidence in the literature that the conversion of tryptophan to N1-methylnicotinamide may require pyridoxine (1,2,3). Holt (4) has suggested that a reduction in the amount of N’-methylnicotinamide excreted after a test dose of tryptophan may be used as a test for pyridoxine deficiency. Other evidence has been reported (5,6), however, that pyridoxine is not a factor of primary importance in the conversion and that the apparent relationship between pyridoxine deficiency and poor conversion of tryptophan to N’-methylnicotinamide is due to severe caloric restriction (6) or protein imbalance (7,8). Heimberg, Rosen, Leder, and Perlzweig (9) have shown that the protein level of the diet is of primary importance to the amount of N’-methylnicotinamide excreted, after test doses of tryptophan; the higher the protein level the lower the amount of N1-methylnicotinamide. They found no evidence to support a primary need for pyridoxine in this conversion, though at a 10% casein level, pyridoxine deprivation induced a reduction in the amount of N’-methylnicotinamide excreted. Using desoxypyridoxine, a pyridoxine antagonist, we have produced what appears to be pyridoxine deficiency in human beings (10). Seborrhea-like dermatitis and mucous membrane lesions are induced which respond to pyridoxine but not to other members of the vitamin B com-