E. A. MacLachlan
Harvard University
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Featured researches published by E. A. MacLachlan.
The Journal of Pediatrics | 1945
James L. Gamble; Kathleen R. Fahey; Janet Appleton; E. A. MacLachlan
Summary Results of study of an infant exhibiting recession of plasma chloride, alkalosis, and a large excess of chloride over sodium in the stools are reported. There was voluminous watery diarrhea which began at birth. The findings indicate, but do not identify, an intrinsic defect in the control of electrolyte distribution in the body fluids.
Journal of Clinical Investigation | 1943
Nathan B. Talbot; Allan M. Butler; E. A. MacLachlan
The evidence of the literature indicates that the adrenal cortex produces a variety of hormones, some of which, like desoxycorticosterone, act predominantly to maintain a normal water and electrolyte balance (1), while others, like corticosterone, are effective chiefly through preventing hypoglycemia, either by facilitating the formation of sugar from protein (gluconeogenesis) (2) or by inhibiting utilization of sugar by the tissues (3). Up to the present, most replacement therapy for patients with adrenal cortical insufficiency has been concerned with these two types of adrenal hormones. There is, however, clinical and experimental evidence that the adrenal cortex also secretes other types of hormones, some of which are androgenic (4, 5). Recent evidence has shown that such androgens not only prompt masculine secondary sexual development, but also an increase in muscular mass and endurance (6, 7). A striking example of this phenomenon is provided by the Herculean development of certain children with virilism due to hyperplasia or carcinoma of the adrenal cortex (8). These individuals usually excrete abnormally large quantities of neutral urinary 17-ketosteroids (9, 10) which are believed to be excretory transformation products of the adrenal cortical and, to a lesser extent, of the testicular androgens (9, 11). A striking example of the effect of adrenal cortical androgens upon a patient with adrenal cortical insufficiency is provided by a boy with congenital adrenal cortical hyperplasia, elevated
The Journal of Pediatrics | 1939
Alfred T. Shohl; Allan M. Butler; Kenneth D. Blackfan; E. A. MacLachlan
Summary Hydrolyzed casein, consisting largely of amino acids, was givenorally to infants as the sole source of nitrogen. The amino acids, in the presence of the non-nitrogenous dietary essentials, gave positive nitrogen balances in all cases. It was also found that positive and sufficient nitrogen balances wereobtained by the intravenous administration of hydrolyzed casein together with glucose and sodium chloride. In most instances, however, there were untoward reactions, most prominently a marked elevation of body temperature. Further study is obviously required to identify and remove the cause of the febrile reactions which in our experience have limited the clinical utility of this form of intravenous nutrition.
The New England Journal of Medicine | 1956
Nathan B. Talbot; John D. Crawford; Charles D. Cook; Mary F. Morrill; E. A. MacLachlan; Anne Heeley
THE neuroendocrine-renal homeostatic mechanisms keep the water and electrolyte content of the body within physiologic limits by adjusting the urinary output of water and solutes in accordance with ...
Experimental Biology and Medicine | 1942
Allan M. Butler; Nathan B. Talbot; E. A. MacLachlan; A. B. Hastings
In his pioneer investigations on perfusion fluids, Ringer observed that while the addition of potassium was not essential for the maintenance of the frog or turtle heart beat. a concentration of approximately 4 milli-equivalents per liter was one of the requisites of a solution providing optimal contractions. For the mammalian heart Locke designated the optimal potassium concentration of perfusion fluids at approximately 5.5 meq. per liter. The observation that potassium salts relieved the paralysis of so-called familial periodic paralysis 1 2 3 4 5 6 and the more recent observation that a fall in serum potassium concentration was associated with the attacks of paralysis suggested a correlation between muscle weakness and serum potassium concentration. 2 3 4 5 6 During such attacks bradycardia, hypotension, arrhythmia and cardiac dilatation have been observed. However, though a fall in the serum potassium concentration occurs with such attacks, the specific concentration at which paralysis appears varies greatly. A somewhat similar concomitant decrease in serum potassium and in muscle strength has been observed following the administration of desoxycorticosterone acetate 7 8 9 10 11 12 13 and the skeletal muscle weakness and the heart failure that may occur with such therapy has been ascribed to these low serum concentrations. 9 , 11 , 13 , 14 On the other hand, low serum potassium levels may occur without paralysis or heart failure following the injection of insulin. 15 , 16 This paper reports the striking fall in serum potassium which we occasionally have observed in patients following the daily administration of either methyl testosterone by mouth or testosterone propionate intramuscularly.
JAMA Pediatrics | 1952
Charles U. Lowe; Mary Terrey; E. A. MacLachlan
Pediatrics | 1950
Lytt I. Gardner; E. A. MacLachlan; Walter Pick; Mary L. Terry; Allan M. Butler
JAMA Pediatrics | 1945
Nathan B. Talbot; Allan M. Butler; Edward L. Pratt; E. A. MacLachlan; J. Tannheimer
The Journal of General Physiology | 1952
Lytt I. Gardner; E. A. MacLachlan; Helen Berman
JAMA Pediatrics | 1943
Nathan B. Talbot; Allan M. Butler; R. A. Berman; P. M. Rodriguez; E. A. MacLachlan