Thiamine distribution in the nervous tissues of human beings, monkeys, rabbits and rats was histochemically studied and the following results were obtained.
1. In the brain, much thiamine is distributed in nerve cells and relatively less in nerve fibres. Thiamine is markedly less in glia cells than in nerve cells.
2. The thiamine content in the nerve cells of the brain and spinal cord are variable according to the locations, functional states and kinds.
3. Much thiamine is detected in the nerve cells of the ganglia, whereas less in the mantle cells. The thiamine contents in these thissues are variable according to the functional states of the cells but scarcely any differences were noted according to the kinds.
4. In the peripheral nerve fibres, much thiamine is detected in the axon and poor in the medullary sheath.
5. Thiamine was found to enter and to leave the Ranvier's node in the peripheral nerve fibres.

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1. A micromethod for fractional determination of vitamin A alcohol and ester was devised and the free and ester forms of the vitamin in serum, milk and liver were determined. Using 1N KOH in 90 per cent ethanol in extraction, the fractional determination could be carried out with practically complete recoveries.
2. With this method it was found that about 90 per cent of vitamin A in human serum was the free form and about 10 per cent the ester form, in agreement with the results obtained previously by the authors.
3. The increase in vitamin A in the serum 3hours after oral administration of vitamin A alcohol or ester is chiefly in the ester form without significant change in the free form.
4. Contrary to the findings of the serum, about 90 per cent of the vitamin in human milk was in the ester form and about 10 per cent in the free form. The ratio was fairly constant whether the milk is taken from the initial, middle or last portion of the congested breast or taken at different times of the day.
5. The levels of vitamin A and ester in the milk after a single oral administration of 33.3mg of A alcohol or ester were highest after 4-6 hours, gradually decreasing thereafter. Whichever form was loaded, it was always the ester that increased significantly, as was the case with serum. There is a slight increase in the free but the rise is insignificant.
6. Of the vitamin A in the liver, about 90 per cent was the ester form and about 10 per cent the free form. The ratio was about the same as in milk.
7. The vitamin A level in the liver 15hours after a single oral administration of 1, 000μg of A alcohol or ester or of 2, 000μg of β-carotene in the mouse was found to be increased in the ester form, the rise being 26.7, 33.6 and 5.3 per cent, respectively. The increase in the free form was slight. The rise in vitamin A in the liver after administration of β-carotene was only about 40 per cent of that following the dose of vitamin A with the same I. U.

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1. Urinary lactic acid excretion rates were determined on human males maintained on a starch wafer diet. Lactic acid levels reached a maximum fours following ingestion of the diet.
2. Thiamine supplementation resulted in a marked diminution in the urinary lactic acid six hours following administration.
3. Pyrithiamine administration resulted in a marked increase in urinary lactic acid excretion fours following ingestion.
4. Pyrithiamine in a 60mg dosage was found to negate the influence of 10mg of thiamine on pyruvate metabolism.
5. Urinary pH changes were consistently decreased with increases in lactic acid excretion. Serum lactic dehydrogenase was decreased in those subjects deficient in thiamine.
6. The data tend to support the concept pyrithiamine blocks the biosynthesis of thiamine pyrophosphate.

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It has been demonstrated that riboflavin deficiency in young guinea pigs is associated with growth retardation, rough hair coats, slight scaling of the skin, and occasionally slight stagger. These symptoms of nutritional deficiency are produced more easily on a high fat ration.
Routine hematological examination of the peripheral blood of the riboflavin-deficient guinea pigs shows that there is no abnormality of the blood picture. Total values as well as those of each fraction of serum proteins also show nothing abnormal.
Microscopically, corneal vascularization, atrophy of the skin, certain nerve changes, such as chromatolysis and myelin degeneration in the pons and spinal cord, and damage of the heart muscle cells were found. The above lesions other than the cardiac lesions were similar to those previously reported for animals of other species. The hearts showed a vacuolar degeneration of the muscle cells characterized by abnormal deposits of glycogen as well as other prominent pathological changes, such as an atrophy of the muscle cells, myocardial hemorrhage and edema. No similar lesios were seen in the control animals, a large number of normal guinea pigs and in those specifically deficient in B vitamins other than riboflavin.

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1. When frozen soy bean curd was soaked in a thiamine solution for a short time, the vitamin disappears from the juice obtained by pressing the curd.
2. This disappearance of thiamine was found neither to be due to oxidation to thiamine disulfide nor to its decomposition by some factors contained in the curd, but to its adsorption on the curd.
3. This adsorption occurs rapidly and tightly.
4. The adsorption increased by denaturation of the protein, whereby a carbonyl group of the protein seems to have some connection.
5. The thiamine adsorbed tightly on the protein could be extracted after hydrolyzing the protein with proteinase.

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1. Analogues of pantothenic acid, i.e., ω-methyl pantothenic acid, pantoyltaurine, ω-methyl pantoyltaurine and analogues of pantethine i.e., ω-methyl pantethine, bis (N-pantoyl-β-aminoethyl) disulfide, bis (N-methyl pantoyl-β-aminoethyl) disulfide, were synthesized and the inhibitory effects of these analogues on lactic acid bacteria were examined and inhibition indexes were calculated.
2. Inhibitory effects of these analogues on germination of higher plants, i.e., “yukina” and barley, were also studied. It was observed that the analogues inhibited the germination and growth of the higher plants, and the inhibitory actions were considerably reversed by the presence of an additional equimolecular amount of pantothenic acid (PaA). Furthermore, the existence of antagoism between pantoic acid, a PaA precursor, and its analogue in the germination of higher plants was shown.
3. The possibility to induce a nutritional deficiency in the chick embryo by injecting PaA analogue, ω-methyl PaA, was found. A lethal dose of ω-methyl PaA on the second day of incubation was 10.0mg per egg and this inhibitory effects were remarkably prevented by a simultaneous injection of PaA. Interference ratio (analogue: vitamin) was roughly 200:1.
4. In the animal experiment, the weight gain of the male DD-strain mice diminished proportionately with the level of supplemented ω-methyl PaA. The inhibitory effects were prevented by a simultaneous addition of PaA. “Interference ratio” was found to be 100:1 to 60:1. Deficiency syndromes induced by ω-methyl PaA were observed.
5. Effects of PaA analogue and pantetheine analogues on the acetylation of sulfanilamide in pigeon liver homogenate were studied. A PaA analogue, ω-methyl PaA, was inert for acetylation, but a pantetheine analogue, ω-methyl pantethine, showed a remarkable inhibition.
6. Effects of these analogues were discussed and the mechanism of their interference action were also discussed.

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1. Male albino rats fed a stock diet supplemented daily with 100mg α-tocopheryl acetate per rat had significantly higher concentrations of CoA, ATP and ADP than did their controls.
2. The significance of these findings is discussed.

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In order to prepare the mycelia of Er. ashbyii as a raw material for extracting FAD, some basal cultural conditions were examined. In these experiments, the FAD stored in the mycelia amounted to 60-120mg/l, and the highest yield obtained was 194mg/l, whereby a shaking culture was used with a medium containing 1% glucose, 1.5% peptone, and 0.1% CSL and incubated for 72hr. In general, with the rise in mycelial growth, the FAD production in the mycelia seems to be decreased.
Preparation of dry mycelia was tested by 3 methods including dehydration with dry acetone and drying by heat. Loss of FAD amounted to about 30% of the initial values. However, the FAD in dried mycelial preparations was stable at least for 6 months in a desiccator. The results of cultures in a 2-ton fermentor were also reported.

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A simplified practical procedure for manufacturing FAD from the mycelia of Eremothecium ashbyii was described. It consists of extraction with pyridine-methanol-water (1:3:1), subsequent adsorption on IRA-401-Cl, followed by washing with a dilute NaCl solution, extraction of FAD with phenol, transfer to water from ether phase, and precipitation with alcohol.

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