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Featured researches published by Gladys A. Emerson.


Experimental Biology and Medicine | 1949

Complete Regression of Lymphosarcoma Implants Following Temporary Induction of Riboflavin Deficiency in Mice.

Herbert C. Stoerk; Gladys A. Emerson

Summary Marked regression of established lymphosarcoma (6 C3H-ED) implants occurred in all of 48 C3H mice rendered temporarily deficient in riboflavin either by the feeding of a diet low in this vitamin or by the administration of an antagonist. In most cases survival was significantly prolonged and 15 mice survived without recurrence of the tumors for more than 200 days. When animals which had survived 60 days or more were reinoculated with lymphosarcoma tissue, the second implant failed to take. Established lymphosarcoma implants in 81 control mice on a diet supplemented with adequate amounts of riboflavin, grew continuously and killed all animals within about 4 weeks.


Experimental Biology and Medicine | 1949

Growth Promoting Activity of Vitamin B12 in Rats Receiving Thyroid Substance

Gladys A. Emerson

Summary Vitamin B12 counteracts the growth retarding effect of thyroid powder when fed in conjunction with a diet devoid of animal protein. The vitamin is equally effective when administered by either the oral or the subcutaneous route.


Experimental Biology and Medicine | 1944

The Antiriboflavin Effect of Isoriboflavin.

Gladys A. Emerson; Max Tishler

Summary The feeding of isoriboflavin to rats receiving a sub-optimal intake of riboflavin inhibited the growth-promoting action of the vitamin. The antagonistic effect of the isomer was prevented or overcome by the feeding of an adequate level of riboflavin.


Archives of Biochemistry and Biophysics | 1955

Changes in coenzyme A concentration during vitamin B12 deficiency

George E. Boxer; C.E. Shonk; Elizabeth W. Gilfillan; Gladys A. Emerson; Evelyn L. Oginsky

Abstract The coenzyme A concentration in the liver and kidney of vitamin B12-deficient rats is 2–3 times higher than in normal or pair-weighed controls. This increase can be demonstrated in male as well as in female animals and is independent of the added stress of thyroid powder feeding. The increase in CoA concentration is due to an increase in the catalytically active, reduced form of CoA. The rate of degradation of CoA is the same in homogenates of livers from deficient and normal animals. Data on the influence of this increase in CoA level on the oxidation of α-ketoglutarate, succinate, pyruvate, and acetate by kidney and liver homogenates are reported. No marked differences were observed with homogenates from B12-deficient or sufficient animals.


Vitamins and Hormones Series | 1948

Vitamins as Pharmacologic Agents

Hans Molitor; Gladys A. Emerson

Publisher Summary This chapter describes the role of fat soluble and water soluble vitamin as pharmacologic agents. Any vitamin may be expected to restore to normal, functional changes which result from the deficiency of that vitamin. It is not easy to determine whether therapeutic results obtained by administration of a vitamin in diseases not following the pattern of a typical deficiency are ascribable to properties other than those necessary for the function as a vitamin. The pure toxic effects of vitamins are those of pyridoxine, which in excessive doses produces clonic-tonic convulsions or of riboflavin. Riboflavin, on repeated intravenous injection of large doses, is precipitated in the glomeruli, thus mechanically interfering with urinary excretion. Certain effects of vitamins cannot be observed by simple inspection or application of the commonly used pharmacologic technics. The pharmacologic effects of vitamins which constitute a restoration to normal of a typical vitamin deficiency are discussed in the chapter. The diagnostic value of vitamin administration is the response to B complex vitamins in cases of “subclinical” deficiency diseases is illustrated. The high specificity of vitamins is demonstrated in experimentally produced pathologic conditions, which resemble those observed in vitamin deficiencies.


Experimental Biology and Medicine | 1942

Biotin Deficiency in the Rat

Gladys A. Emerson; John C. Keresztesy

Summary Synthetic pyridoxine is almost inactive as a growth factor for S. Zizctis Rin a pyridoxine-free medium if heat sterilization is avoided. Autoclaving media which contain pyridoxine greatly increases its activity for this organism. The same effect was achieved in varying degrees by autoclaving pyridoxine at neutrality with individual amino acids. Cystine and glycine were most effective in producing this change.


Experimental Biology and Medicine | 1954

Effect of Intrinsic Factor Concentrate upon Utilization of Orally Administered Vitamin B12 by Rats.

Charles Rosenblum; David T. Woodbury; Elizabeth W. Gilfillan; Gladys A. Emerson

Summary 1. The effect of a clinically active intrinsic factor concentrate on the absorption of cobalt 60 labeled vit. B12 by rats after oral administration has been studied. 2. Measurements of the radioactivity of kidneys, livers and urine indicate lowered absorption in the presence of intrinsic factor concentrate. Fecal radioactivity is too variable to permit reliable conclusions. 3. Injection of a massive dose (20 μg) of normal B12 4 days after oral administration of the labeled vitamin liberates additional urinary radioactivity, and again points to an inhibitory effect of intrinsic factor concentrate.


Experimental Biology and Medicine | 1945

Non-Availability of Fecal Thiamine in Thiamine Deficiency

Gladys A. Emerson; Harry G. Obermeyer

Summary Rats maintained on a thiamine-deficient diet excreted essentially the same concentration of thiamine in their stools as did animals receiving 5 or 50 μg of thiamine daily. The output of feces was greatly reduced in the thiamine low group. During the later stages of the depletion the thiamine was present largely in the form of cocarboxy-lase. The fecal thiamine of the deficient rats was not available when administered curatively by the oral route to animals which had plateaued in weight on a thiamine-low diet.


Experimental Biology and Medicine | 1944

Biotin-Pantothenic Acid Interrelationship in Rats Fed Succinylsulfathiazole:

Gladys A. Emerson; Elizabeth Wurtz

Summary Biotin deficiency induced in weanling rats by the feeding of a succinylsulfathiazole containing purified ration may be aggravated by superimposing a deficiency of pantothenic acid. The feeding of biotin protected against these changes and, in addition, appeared to lessen the severity of the syndrome associated with a lack of pantothenic acid. Calcium pantothenate, fed prophylactically, was completely protective against deficiency signs usually associated with the absence of pantothenic acid. Furthermore, signs of a mild degree only of biotin depletion were observed and the period required to produce such changes was extended beyond that observed in the absence of pantothenic acid. Rats receiving both biotin and calcium pantothenate were free from signs of both deficiency states.


Experimental Biology and Medicine | 1945

Fecal Riboflavin of Rats Receiving Varying Intakes of Riboflavin

Harry G. Obermeyer; Elizabeth Wurtz; Gladys A. Emerson

Summary The concentration of riboflavin in the stools of young rats maintained on a riboflavin deficient diet or at intakes of 10 μg or 40μg of this vitamin per day remained constant throughout a test period of 40 days and was essentially the same for all groups. The total output of riboflavin was dependent upon the quantity of feces excreted. Rats receiving riboflavin but with the caloric intakes restricted to the extent of 50% excreted less total riboflavin than did their ad libitum controls. Addendum. After this paper had been accepted for publication, Schweigert et al. 8 reported that cecectomized rats on complete synthetic rations and synthetic rations containing limited amounts of the individual B vitamins grew at the same rate as their controls. They concluded that growing rats on sucrose-containing diets did not depend to any extent on the cecum for the absorption or synthesis of these known or required factors.

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