89cells shrink considerably. Erythrocytes show a similar but smaller shift both of electrolytes and water.Indoleacetic acid also causes shrinkage of the tumor cells, and loss of potassium chloride. With erythrocytes the effect was quite small, although definite shrinking was seen (3). In correspondence the indoleacetate ion showed a smaller effect than pyridoxal in the present experiments ( Fig. 1 ) .Evidence obtained with tumor cells from pyridoxine-deficient mice implicates pyridoxal in the normal process of amino acid accumulation by these cells (3,4). A close relationship to the transfer of potassium into cells is also indicated (3).
Summary. Pretreatment of erythrocyteswith 10 m M pyridoxal makes the cells subsequently more-resistant to lysis by hypotonic solutions. Indoleacetic acid shows the same behavior to a smaller degree. These effects are attributed to a net loss of cell solutes in the form of potassium and chloride which the agents produce.
In 1934 Gybrgy (1.) announced the existence of an essential vitamin for the rat which was distinct from vitamins B1 and B2. He called it the "antiacrodynia" factor. For a while it carried the name "Adermin" because rats deficient in this substance developed dermatitis, but after its synthesis in 1939 by Harris and Folkers (2) it was renamed pyridoxine. Thereafter numerous reports appeared concerning deficiency states in various animals deprived of this essential nutrient. Deprivation experiments in human beings have not produced clear-cut clinical results and human pyridoxine requirements are unknown.
1. The hematologic syndrome called refractory anemia with hyperplastic bone marrow, aregenerative anemia, chronic bone marrow failure, pseudo-aplastic anemia, and many other terms, has been separated into five types on the basis of clinical and hematologic studies on 23 patients carried out over a period of 16 years. These groupings are probably highly artificial but are made to facilitate presentation and description. As more is learned of the chemistry of the bone marrow cells in patients with refractory anemia, a more satisfactory classification will be possible.
2. Type 1 is characterized by bizarre chromatin in the normoblasts, mast cell hyperplasia, hemosiderosis or hemochromatosis and a tendency for spontaneous remissions to occur.
3. Type 2 is at first typified by complete or almost complete erythroid aplasia. Hyperplasia of erythroid cells with maturation arrest and bizarre chromatin pattern may occur later, and finally spontaneous remission may appear with considerable frequency. Mast cell hyperplasia, thymoma and hemosiderosis have been noted.
4. Type 3, associated with exogenous toxins and the preleukemia state, is characterized by pancytopenia and a bizarre chromatin pattern in the normoblasts. Some of these patients may he classified as "DiGuglielmo syndrome."
5. Type 4 also is typified by pancytopenia and hyperplasia of bone marrow but with cells of normal appearance. These patients responded partially or completely when splenectomy was performed, and probably represent a variant of the "hypersplenism" syndrome.
6. Type 5 is refractory megaloblastic anemia with typical cytologic changes evident in all cell types similar to those found in pernicious anemia.
7. Hypotheses are proposed to explain these various types of anemia on the basis of abnormalities in the metabolism of nucleic acids, particularly DNA. Deficiencies of metabolites, inhibition of metabolic reactions by exogenous or endogenous toxins, or by immune mechanism in which DNA serves as haptene, are possible explanations.
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