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These authors have produced myelopathy in the albino rat in a variety of ways: by vitamins B1, E, and H (biotin) deficiency diets, extirpation of the gastric mucosa, intoxication by monoiodoacetic acid (Lasazt and Verizár assumed that the intoxication inhibits growth through stopping the phosphorylation of riboflavin, ie, its turning into active vitamin B2), alcohol, carbon tetrachloride (cleaning agent in households), lathyrus seeds, triorthocresyl phosphate (which the authors consider responsible for "ginger paralysis"), and sulphonamides. The same effect has been produced in alloxan and dithizon diabetes, in "hyperthyroidosis" (administering thyroxin), and in animals fed α-thioproprionic acid disulphide (an antimetabolite, "competitive antagonist of each of methionine, cystine, and glutamic acid") and 2, 4-dichlorphenoxyacetic acid (a "weed extirpator"). The only experiments undertaken in which they failed to produce myelopathy were those in rats fed p-nitrobenzoyl glutamic acid ("an antimetabolite of glutamic acid") in which neuronal degeneration occurred. In this