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Biographical Memoirs: Volume 63 This page in the original is blank.
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Biographical Memoirs: Volume 63 ALBERT BAIRD HASTINGS November 20, 1895–September 24, 1987 BY HALVOR N. CHRISTENSEN A. BAIRD HASTINGS was born in Dayton, Kentucky. When he was six years old, his family moved to Indianapolis, where he lived until he entered college. His father died of tuberculosis while Baird was in his second year of high school. No special interest in science was uncovered in Baird's study at Shortridge High School, where he liked Greek and Latin and aspired to become a classics teacher. Upon the death of his father, Baird prepared to leave high school to help support his family. The teacher who had profoundly inspired him, Ella Marthens, urged otherwise, however, and she helped to arrange an assistantship in biology for him, given only that he should take a course in zoology. Subsequently, mathematics through solid geometry and physics, but no chemistry, supplemented that obliged biology study. Baird remarked how frequently career success is attributed to the influence of a superior high school teacher rather than to college teachers. Baird told of a notable evening in his senior year at the home of Marthens and a teaching colleague, attended by Baird's favorite crony and classmate, Alan Boyd, at which a group decision was to be reached about Baird's college attendance. Baird insisted that it be at Michigan, where two cousins, James and Charles Baird, had attended and
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Biographical Memoirs: Volume 63 had, among other distinctions, played and coached football, respectively. Under the assumption that Baird must quickly learn to make a living to help his family, the group decided that he must register for engineering, specifically chemical engineering, a subject unfamiliar enough to avoid any perceived limitation in Baird's abilities. His first encounter with the required general chemistry did not yet divert him from engineering. Odd jobs of various sorts helped family finances, and the second marriage of his mother made further borrowing unnecessary. But in the summer after his second year, Baird liked very much more the physical chemistry course under Dr. Floyd Bartell that he had included in his program. At the end of this course, Bartell asked Baird if he would like to serve as his assistant in the physical chemistry course. The assistant had to prepare the apparatus and solutions needed and also help with instructing the students in the laboratory. The offer required, however, that Baird become a major in chemistry, a shift only slowly and reluctantly accepted by the engineering school, indeed by default, and, as it happened, with an unjust discount of Baird's prior marks. Among the provisions of this post was a 20 × 20 foot laboratory belonging to Bartell, which adjoined his own lab. As Baird remarked, "That was in the fall of 1915, and from that moment until 1966, I've had a laboratory of my own. This provision has determined everything I've done since."1 DOCTORAL STUDY SUPPORT BY THE PUBLIC HEALTH SERVICE At the end of 1916, Baird had taken all the courses, undergraduate and graduate, offered in physical chemistry, so Bartell asked him what he would do upon graduation. Baird supposed he would get a job, not difficult
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Biographical Memoirs: Volume 63 then. Bartell instead urged him to go on with graduate work. Baird expostulated: "You mean work for a Ph.D.? That's ridiculous! You have to be a Van't Hoff to do that." Bartell responded, "I've watched you, Baird, and I find you work hard and are resourceful." In his life story Baird commented that he accepted this evaluation as a watchword. "I tried ever after to be resourceful in the lab." He was able to enter graduate school in January 1917, even though he was not scheduled to receive his baccalaureate degree until June. Since there was no more physical chemistry to take, he elected to begin graduate courses with some advanced quantitative chemistry, minerology, and bacteriology under F. G. Novy. Because Bartell was interested in membranes and osmosis, Baird proceeded with preliminary research on the permeability of collodian membranes. Thus, membrane studies became the beginning of his lifelong interest in the distribution of solutes in heterogeneous systems. Another event, the appearance of Bayliss's Principles of General Physiology , a remarkable book in its first edition, stimulated Baird's interest toward biological subjects, just when his interest had been narrowing to physical chemistry. But in April 1917 the United States entered World War I, with strong consequences for the direction of Baird's progress. As most of his friends left to go to camp, the underweight Baird began a desperate campaign to enlist. By the fall of 1917, his persistent efforts to be accepted into the military having failed, Baird returned to the University of Michigan. His Ph.D. study in physical chemistry was, however, deferred (permanently, as it happened) because Bartell himself was about to take a commission in the Chemical Warfare Service. Therefore, Baird helped Bartell in his course in the fall of 1917 as an instructor. A
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Biographical Memoirs: Volume 63 chance encounter with Hector Britton, who held a summer post as a chemist with the Public Health Service working on a multidisciplinary study of fatigue, led Baird to take Britton's place (on being reassured that this was indeed war work) when the latter returned to his Ph.D. study in organic chemistry. Officialdom was tending at this point to conclude that fatigue as encountered in munitions plants was due to acidosis. Baird's experience in setting up and using the Hildebrand bubbling hydrogen electrode persuaded Joseph W. Schereschewsky of the Public Health Service that Baird probably knew as much as anyone about the measurement of the state of neutrality. Baird liked to say that his whole life story was essentially determined when he accepted the post as sanitary chemist with the Public Health Service on November 1, 1917, to study these matters. "Everything else followed logically," he said. Although he had no study in physiological science up to that point, Baird quickly perceived that physiological neutrality was not a simple subject. His initial assignment was to measure the pH of morning and evening urine of workers engaged in various operations at the Ford Motor Company. By mid-December, even though Kjeldahls and measures of free and conjugated phenols and of three kinds of sulfur had been added, he was ready to write a letter to Frederic S. Lee, head of physiology at Columbia University, who was directly in charge of Baird's activity, to the effect that the program was no way to study fatigue, that it was a waste of federal money and of his time, and that, unless the government was prepared to study fatigue in animals under controlled laboratory conditions, he did not want to proceed. From that letter came orders for him to proceed to the Department of Physiology at Columbia and to carry out research on the chemistry of fatigue. The logical progression continued.
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Biographical Memoirs: Volume 63 Baird wrote that nobody ever had better tutorial training than he received in that department. Beyond Frederic Lee, he acknowledged how much he came to owe Professors F. H. Pike, Russell Burton-Opitz, and Ernest L. Scott. When the war ended, Lee invited Baird to continue for a Ph.D. degree. Baird pointed out that he had expected to return to Ann Arbor to go on with his studies for a Ph.D. degree in physical chemistry with Bartell. The decisive circumstance was that Baird and Margaret Hastings were married May 31, 1918, and that on May 14, 1919, their son Alan Baird Hastings was born. The ongoing Public Health Service stipend of $2,400 was twice the Michigan stipend. So on the grounds of economic need, Baird decided to become a physiologist. "It had nothing to do with the desire to become a physiologist"—a strange admission in light of his subsequent lifelong affinity for physiology. Ernest L. Scott became his immediate thesis adviser. With Scott he completed the studies that each of them had separately initiated on sulfur and phenol metabolism. Baird's results were then published in Public Health Service reports as his first papers. In the meantime he continued his study of what would subsequently be called changes in the acid-base balance as the result of exercise. Columbia University was generous in accepting Michigan's credits for Baird's interrupted courses. To earn the needed initial credits in physiology, Baird assisted in teaching the laboratory course. For biochemistry, since not much time could be spared from his remunerated research, he attended a course that met all day Saturday in the second semester for medical students who had failed their course the preceding semester. As Baird noted, "And that is all the formal biochemistry I ever had." Can the sort of biochemistry he missed up to 1921 help us appraise his total influence on this emerging science?
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Biographical Memoirs: Volume 63 Baird's thesis research also included a part on changes in the fragility of red blood cells upon exercise, a quickly successful problem suggested by Scott. They found that after a prolonged period without exercise the blood of a dog accumulates a lot of old red blood cells, about to be broken up. Strong exercise broke up these doomed blood cells faster than the spleen could remove them, leading to the pink plasma of a hemoglobinemia. The project also involved observing changes in red blood cell fragility arising from blood oxygenation and reduction and from CO2 addition and extraction. This work brought Baird's interest into the osmotic consequences of changes in the distribution of chloride and bicarbonate, an interest greatly extended later at the hospital of the Rockefeller Institute. In his concurrent attempts to study the alkali reserve of blood plasma in exercise and fatigue, Baird adapted a hydrogen electrode, one previously described by J. B. McClendon, for titrating the plasma to measure the alkali reserve. He wrote up this procedure and the particular electrode adaptation with the idea that it might be published. He brought it along to consult with his friend, Dr. Glenn E. Cullen, who was then Van Slyke's first assistant at the hospital of the Rockefeller Institute. Cullen was pleased with it and at once took it into Van Slyke's office. Cullen soon came out and said, "Dr. Van Slyke wants to see you." Van Slyke, then editor of the Journal of Biological Chemistry, accepted the paper for publication then and there, on March 9, 1921. ROCKEFELLER INSTITUTE PERIOD Van Slyke then asked Baird what he planned to do upon completion of his Ph.D. Van Slyke approved his intent to proceed to Washington, D.C., to develop the Public Health Service program in physiology for which Schereschewsky
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Biographical Memoirs: Volume 63 had arranged his training. Van Slyke also emphasized the accompanying possibility of an association there with the newly appointed William Mansfield Clark. But then Van Slyke added, "There might be another possibility—don't do anything until you hear from me." Baird waited from March until June for Van Slyke to feel free to propose that Baird become his first assistant—"probably the best job in the country in 1921 for a fresh Ph.D." It placed Baird in charge of Van Slyke's research labs. The experiments were planned together, but the organization and execution were in Baird's hands. Ever afterward, however, Baird had a guilty feeling that he had let down Schereschewsky, who had left him at Columbia to finish his Ph.D. so that Baird could start the Department of Physiology at the National Hygienics Laboratory. "My guilt accounted for my willingness from that moment to do anything that the Public Health Service asked me to do," Baird said. In Van Slyke's lab, Baird's associates began at once to call him a biochemist, a name he did not deny, even though "I knew in my heart I wasn't one." Clearly, Baird then followed Van Slyke's prior example upon his earlier arrival at the institute with arduous study to deserve this name. Baird joined with Van Slyke, John Plazin, Michael Heidelberger, James M. Neill, and occasional visitors in the so far unsuccessful attempts to clearly delineate differences in the CO2 absorption curves of oxygenated and reduced blood. One day the frustrating technical difficulty brought Baird and Neill out into Central Park for relief. In the ensuing conversation, it was obviously Baird who proposed the subsequently familiar two-compartment system for equilibrating blood and a desired gas phase, to allow separation of these phases for analysis without dis-
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Biographical Memoirs: Volume 63 turbing the equilibrium. This simple but resourceful device greatly accelerated progress in the lively program that ensued. Baird would stay overnight in the hospital, sleeping in an in-a-door bed so that he could start the experiments at 7 a.m. and have samples ready for analysis in an hour and a half when the rest of the team arrived. By 10 or 11 the same evening, the data would have been calculated and plotting begun. Now the plots became remarkably consistent, and subsequent productivity became equally remarkable. So the laboratory study of the acid-base balance of blood entered a rich phase on its way to becoming an ultimate classic as described in 1932, in Quantitative Clinical Chemistry by Peters and Van Slyke. "Van Slyke always said that this was the happiest and most productive time of his life, and it certainly was for me," Baird said. He further regarded the next five years he spent in Van Slyke's laboratory as the most important experience he ever had. The quality of that experience stands clear in his National Academy of Sciences' memoir for Van Slyke in 1976, although Baird's five years of participation are scarcely mentioned. In describing this rich experience, Baird also emphasized the significance of his placement, along with that of Van Slyke, the only two biochemists among a half dozen clinicians engaged in important clinical research. Thus, early in his career he learned not only to respect but also to be sympathetic toward clinical investigators and their clinical problems. "This, perhaps more than what I learned in biochemistry, determined my future," Baird said. He also noted the importance of the output from the Hospital of the Institute of numerous people who became leading professors of medicine—for example, Walter W. Palmer, Oswald H. Robertson, Franklin McLean, and C. Phillip Miller, Jr.
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Biographical Memoirs: Volume 63 Baird held that "the quantitative study of disease was born to a considerable degree at the Rockefeller Institute." Tosteson quotes Baird as saying much later, "Whatever biochemistry is today—it owes as much to clinical medicine for its high place among the biological sciences—as medicine owes to it." During these five years, Baird also initiated his studies of the physiochemical basis for bone deposition, in particular by a pioneering application of the DeBye-Huckel theory to the stepwise dissociation of carbonic and phosphoric acids. In the spring of 1925, Flexner asked Baird, now an associate, to supervise a two-week visit by Otto Warburg. Baird was commissioned, upon learning to use the Warburg apparatus for measuring tissue respiration, to teach its use in the Cancer Research Laboratory of the Institute. Baird told the story of how it became obvious to him that Warburg had heretofore in his work not measured the pH but calculated the hydrogen ion concentrations, all the while assuming exactly concurrent rather than successive dissociation of the two hydrogen ions of carbonic acid. On Warburg's return to Germany he published a brief correction with thanks to Hastings. Furthermore, he invited Hastings to Berlin-Dahlem, and, during the following summer stay by the young Hastings family, Baird learned to his pleasure the use of the gold-leaf electroscope, actually for measuring the coefficient of solubility of radon in yeast cells and red blood cells. Baird always gave his wife, Margaret Johnson Hastings, much credit for inspiring him with her high academic standards and with helping him make career decisions throughout their lives together. Margaret proposed the Sunday teas at which the Hastings later entertained first-year Harvard medical students. Members of Baird's department also were ben-
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Biographical Memoirs: Volume 63 eficiaries of her gracious hospitality. As Buchanan remarks in his preface to Crossing Boundaries, the Hastings lived courtly and elegant lives. They maintained close associations with numerous relatives and friends, as their musical and artistic son, also named Baird, recounted. UNIVERSITY OF CHICAGO PERIOD In 1926, Baird took wing by accepting a professorship in the Department of Physiological Chemistry at the University of Chicago. A year and a half later his professorship was transferred to the Department of Medicine with the creation of the first of the two successive Lasker foundations. "I had a staff of three and $50,000 of hard money to spend," namely on the study of degenerative disease, Baird said. After an earlier excursion with Harold B. Van Dyke to compare the blood distribution of bromide as a function of pH with that of the previously studied chloride ion, Hastings undertook the major problem of describing the movement of water and ions between the extra-and intracellular phases of muscle and other tissues. The first problem was to figure out how to determine what fraction of a piece of tissue is extracellular and what portion is intracellular, and even whether the extracellular fluid portion could be considered an ultrafiltrate of the blood plasma. First, Baird had to escape from the prejudice that the Donnan equilibrium would sufficiently account for the distribution of ions. Only when he and Lillian Eichelberger showed that muscle cells are not freely permeable to ions, and contained little or no chloride ion, had they struck a productive track. Wallace Fenn, J. P. Peters, and Daniel Darrow were then approaching the same conclusion about muscle. The same approach proved applicable to liver and heart, although the inhomogeneity of kidney and brain
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Biographical Memoirs: Volume 63 With E. L. Compere and F. C. McLean. State of calcium in the fluids of the body. II. Calcium in the blood in rickets. Am. J. Dis. Child. 50:77–83. With F. C. McLean and B. O. Barnes. The relation of the parathyroid hormone to the state of calcium in the blood. Am. J. Physiol. 113:141–49. With F. W. Schlutz and M. Morse. Acidosis as a factor of fatigue in dogs. Am. J. Physiol. 113:595–601. With N. W. Shock. Studies of the acid-base balance of the blood. IV. Characterization and interpretation of displacement of the acid-base balance. J. Biol. Chem. 112:239–62. 1936 With J. E. Davis. The effect of thyroxin on the tissue metabolism of excised limulus heart. Am. J. Physiol. 114:618–19. With E. G. Weir. The ionization constants of calcium proteinate determined by the solubility of calcium carbonate. J. Biol. Chem. 114:397–406. 1937 With L. Eichelberger. The exchange of salt and water between muscle and blood. I. The effect of an increase of total body water produced by the intravenous injection of isotonic salt solutions. J. Biol. Chem. 117:73–93. With L. Eichelberger. The exchange of salt and water between muscle and blood. II. The effect of respiratory alkalosis and acidosis induced by overbreathing and rebreathing. J. Biol. Chem. 118:197–204. With L. Eichelberger. The exchange of salt and water between muscle and blood. III. The effect of dehydration. J. Biol. Chem. 118:205–15. With E. H. Stotz. The components of the succinate-fumarate enzyme system. J. Biol. Chem. 118:479–98. With A. A. Browman. Solubility of aragonite in salt solutions. J. Biol. Chem. 119:241–46.
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Biographical Memoirs: Volume 63 1938 With F. J. Mullin and W. M. Lees. Neuromuscular responses to variations in calcium and potassium concentrations in the cerebrospinal fluid. Am. J. Physiol. 121:719–27. With H. I. Chu. A note on the state of calcium in high protein serum. J. Clin. Invest. 17:167–68. With F. W. Klemperer and H. C. Trimble. The uricase of dogs, including the Dalmatian. J. Biol. Chem. 125:445–48. With J. F. Manery. The distribution of electrolytes in mammalian tissues. J. Biol. Chem. 127:657–76. With D. J. Cohn, A. Tannenbaum, and W. Thalhimer. Influence of oxygen and carbon dioxide on the blood of normal and pneumonic dogs. J. Biol. Chem. 128:109–31. With J. M. Muus and O. A. Bessey. Tissue metabolism in vitamin deficiencies. I. Effects of deficiencies in riboflavin and other heat stable vitamin B components. J. Biol. Chem. 129:295–301. With J. M. Muus and S. Weiss. Tissue metabolism in vitamin deficiencies. II. Effect of thiamine deficiency. J. Biol. Chem. 129:303–7. With E. G. Weir. The distribution of bromide and chloride in tissues and body fluids. J. Biol. Chem. 129:547–58. With I. S. Danielson. A method for determining tissue carbon dioxide. J. Biol. Chem. 130:349–56. With I. S. Danielson and H. I. Chu. The pK' of carbonic dioxide in concentrated protein solutions and muscle. J. Biol. Chem. 131:243–57. With H. L. Blumgart, O. H. Lowry, and D. R. Gilligan. Chemical changes in the heart following experimental temporary coronary occlusion. Trans. Assoc. Am. Physicians 54:237–43. With N. Drinker and A. A. Greene. Equilibria between calcium and purified globulins. J. Biol. Chem. 131:649–62. With J. F. Taylor. Oxidation-reduction potentials of the methemoglobin–hemoglobin system. J. Biol. Chem. 131:649–62.
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Biographical Memoirs: Volume 63 1940 With M. Kiese. Factors affecting the activity of carbonic anhydrase. J. Biol. Chem. 132:281–92. With D. D. Van Slyke, A. A. Hiller, D. A. McFadyen, and F. W. Klemperer. On hydroxylysine. J. Biol. Chem. 133:287–88. With H. N. Christensen. Phosphatides and inorganic salts. J. Biol. Chem. 136:387–98. The electrolytes of tissues and body fluids. Harvey Lectures 36:91–125. With J. B. Conant, R. D. Cramer, F. W. Klemperer, A. K. Solomon, and B. Vennesland. Metabolism of lactic acid containing radioactive carboxyl carbon. J. Biol. Chem. 137:557–66. With B. J. Jandorf and F. W. Klemperer. A manometric method for the determination of diphosphopyridine nucleotide. J. Biol. Chem. 138:311–20. With J. O. Hutchens, and B. J. Jandorf. Synthesis of diphosphopyridine nucleotide by chilomonas paramecium. J. Biol. Chem. 138:321–25. With A. K. Solomon, B. Vennesland, and J. M. Buchanan. The participation of carbon dioxide in the carbohydrate cycle. J. Biol. Chem. 140:171–82. With B. Vennesland, A. K. Solomon, J. M. Buchanan, and R. D. Cramer. Metabolism of lactic acid containing radioactive carbon in the a or ß position. J. Biol. Chem. 142:371–77. With B. Vennesland, A. K. Solomon, and J. M. Buchanan. Glycogen formation from glucose in the presence of carbon dioxide. J. Biol. Chem. 142:379–85. With O. H. Lowry. Histochemical changes associated with aging. I. Methods and calculations. J. Biol. Chem. 143:257–69. With O. H. Lowry, T. Z. Hull, and A. N. Brown. Histochemical changes associated with aging. II. Skeletal and cardiac muscle in the rat. J. Biol. Chem. 143:271–80. With O. H. Lowry, C. M. McCay, and A. N. Brown. Histochemical changes associated with aging. III. The effects of retardation of growth on skeletal muscle. J. Biol. Chem. 143:281–84. With F. W. Klemperer and D. D. Van Slyke. The dissociation constants of hydroxylysine. J. Biol. Chem. 143:433–37. With O. H. Lowry and D. R. Gilligan. Histochemical changes in the
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Biographical Memoirs: Volume 63 myocardium of dogs following experimental temporary coronary arterial occlusion. Am. J. Physiol. 136:474–85. With J. F. Taylor. The equilibrium between oxygen and hemoglobin in concentrated urea solution. J. Biol. Chem. 144:637–49. With W. M. Wallace. The distribution of the bicarbonate ion in mammalian muscle. J. Biol. Chem. 144:637–49. With C. B. Anfinsen and O. H. Lowry. The application of the freezing-drying technique in retinal histochemistry. J. Cell. Comp. Physiol. 20:231–37. With J. M. Buchanan and F. B. Nesbett. Glycogen formation from pyruvate in vitro in the presence of radioactive carbon dioxide. J. Biol. 145:715–16. With J. M. Buchanan. The role of intracellular cations on liver glycogen in vitro . Proc. Natl. Acad. Sci. USA 28:476–82. 1943 With H. Tabor. The ionization constant of secondary magnesium phosphate. J. Biol. Chem. 148:627–32. With J. M. Buchanan and F. B. Nesbett. The role of carboxyl-labeled acetic, propionic, and butyric acids in liver glycogen formation. J. Biol. Chem. 150:413–25. 1944 With W. W. Westerfeld, J. R. Weisiger, and B. G. Ferris. The production of shock by callicrein. Am. J. Physiol. 142:519–40. 1946 With M. B. Shimkin. Medical research mission to the Soviet Union. Science 103:605–8, 637–44. With O. H. Lowry, C. M. McCay, and A. M. Brown. Histochemical changes associated wih aging. IV. Liver, brain, and kidney in the rat. J. Gerontol. I:345–57. 1947 With C. B. Anfinsen, A. E. Beloff, and A. K. Solomon. The in vitro turnover of dicarboxylic amino acids in liver slice proteins. J. Biol. Chem. 168:771–72. With H. W. Deane, F. B. Nesbett, and J. M. Buchanan. A cytochemi-
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Biographical Memoirs: Volume 63 cal study of glycogen synthesized from glucose or pyruvate by liver slices in vitro. J. Cell. Comp. Physiol. 30:255–64. 1948 With R. B. Singer. An improved clinical method for the estimation of disturbances of the acid-base balance of human blood. Medicine 27:223–42. 1949 With R. G. Gould, F. M. Sinex, I. N. Rosenberg, and A. K. Solomon. Excretion of radioactive carbon dioxide by rats after administration of isotopic bicarbonate, acetate, and succinate. J. Biol. Chem. 177:295–301. With A. K. Solomon, C. B. Anfinsen, R. G. Gould, and I. N. Rosenberg. Incorporation of isotopic carbon dioxide in rabbit liver glycogen in vitro. J. Biol. Chem. 177:717–26. With R. G. Gould, C. B. Anfinsen, I. N. Rosenberg, A. K. Solomon, and Y. J. Topper. Metabolism of isotopic pyruvate and acetate in rabbit liver slices in vitro. J. Biol. Chem. 177:727–31. With C. A. Villee. Metabolism of C14-labeled glucose by the rat diaphragm in vitro. J. Biol. Chem. 179:673–87. With Y. J. Topper. A study of the chemical origins of glycogen by use of C14-labeled carbon dioxide, acetate, and pyruvate. J. Biol. Chem. 179:1255–64. With J. M. Buchanan and F. B. Nesbett. The effect of the ionic environment on the synthesis of glycogen from glucose in rat liver slices. J. Biol. Chem. 180:435–45. With J. M. Buchanan and F. B. Nesbett. The effect of the ionic environment on the synthesis of glycogen and total carbohydrate from pyruvate in liver slices. J. Biol. Chem. 180:447–55. With O. H. Pearson and H. Bunting. Metabolism of cardiac muscle: Utilization of C14-labeled pyruvate and acetate by rat heart slices. Am. J. Physiol. 158:251–60. With O. H. Pearson, C. K. Hsieh, and C. H. DuToit. Metabolism of cardiac muscle: Utilization of C14-labeled pyruvate and acetate in diabetic rat heart and diaphragm. Am. J. Physiol. 158:261–68. With C. A. Villee. The utilization in vitro of C14-labeled acetate and pyruvate by diaphragm muscle of rat. J. Biol. Chem. 181:131–39. With C. A. Villee and H. W. Deane. The synthesis of glycogen in vitro by rat diaphragm muscle. J. Cell. Comp. Physiol. 34:159–70.
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Biographical Memoirs: Volume 63 1950 With J. W. Raker, I. M. Taylor, and J. M. Weller. Rate of potassium exchange of the human erythrocyte. J. Gen. Physiol. 33:691–702. With E. B. Flink and J. K. Lowry. Changes in potassium and sodium concentrations in liver slices accompanying incubation in vitro. Am. J. Physiol. 163:598–604. 1951 With C. B. Mueller. The rate of transfer of phosphorus across the red cell membrane. J. Biol. Chem. 189:869–79. With C. B. Mueller. Glycolysis and phosphate fractions of red blood cells. J. Biol. Chem. 189:881–88. With C. P. Lyman. The total CO2, plasma pH, and pCO2 of hamsters and ground squirrels during hibernation. Am. J. Physiol..167:633–37. 1952 With C. T. Teng, F. B. Nesbett, and F. M. Sinex. Studies on carbohydrate metabolism in rat liver slices. I. The effect of cations in the media. J. Biol. Chem. 194:68–81. With C. T. Teng, F. M. Sinex, and H. W. Deane. Factors affecting glycogen synthesis by rat liver slices in vitro. J. Cell. Comp. Physiol. 39:73–88. With C. A. Villee and V. K. White. The metabolism of C14-labeled glucose and pyruvate by rat diaphragm muscle in vitro. J. Biol. Chem. 195:287–97. With I. M. Taylor and J. M. Weller. The effect of choline esterase and choline acetylase inhibitors on the potassium concentration gradient and potassium exchange of human erythrocytes. Am. J. Physiol. 168:658–65. With F. M. Sinex and J. MacMullen. The effect of insulin on the incorporation of carbon-14 into the protein of rat diaphragm. J. Biol. Chem. 198:615–19. 1953 With C. T. Teng, M. L. Karnovsky, B. R. Landau, and F. B. Nesbett. Metabolism of C14-labeled glycerol and pyruvate by liver in vitro. J. Biol. Chem. 202:705–16. With R. Z. Dintzis. The effect of antibiotics on urea breakdown in mice. Proc. Natl. Acad. Sci. USA 39:571–78.
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Biographical Memoirs: Volume 63 With A. E. Renold, C. T. Teng, and F. B. Nesbett. Studies on carbohydrate metabolism in rat liver slices . II. The effect of fasting and of hormonal deficiencies. J. Biol. Chem. 204:533–46. With A. E. Renold and C. T. Teng. Cationic and hormonal influences on carbohydrate metabolism of rat liver in vitro. Trans. Assoc. Am. Physicians 66:129–36. 1954 With E. Calkins and I. M. Taylor. Potassium exchange in the isolated rat diaphragm; effect of anoxia and cold. Am. J. Physiol. 177:211–21. With A. E. Renold and F. M. Nesbett. Studies on carbohydrate metabolism in rat liver slices. III. Utilization of glucose and fructose by liver from normal and diabetic animals. J. Biol. Chem. 209:687–96. With J. Ashmore and F. B. Nesbett. The effect of diabetes and fasting on liver glucose-6-phosphatase. Proc. Natl. Acad. Sci. USA 40:673–78. 1955 With A. E. Renold, F. B. Nesbett, and J. Ashmore. Studies on carbohydrate metabolism in rat liver slices. IV. Biochemical sequence of events after insulin administration. J. Biol. Chem. 213:135–46. With B. R. Landau and F. B. Nesbett. Origin of glucose and glycogen carbons formed from C14-labeled pyruvate by livers of normal and diabetic rats. J. Biol. Chem. 214:525–35. With J. Ashmore, A. E. Renold, and F. B. Nesbett. Studies on carbohydrate metabolism in rat liver slices. V. Glycerol metabolism in relation to other substrates in normal and diabetic tissue. J. Biol. Chem. 215:153–61. 1956 With A. Ames III. Studies on water and electrolyte in nervous tissues. I Rabbit retina incubated in vitro: Methods and interpretation of analytical data. J. Neurophysiol. 19:201–12. With J. Ashmore, F. B. Nesbett, and A. E. Renold. Studies on carbohydrate metabolism in rat liver slices. VI. Factors influencing glucose-6-phosphatase. J. Biol. Chem. 218:77–88. With J. Ashmore, J. Kinoshita, and F. B. Nesbett. Studies on carbohydrate metabolism in rat liver slices. VII. Evaluation of the Emb-
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Biographical Memoirs: Volume 63 den-Meyerhoff and phosphogluconate oxidation pathway. J. Biol. Chem. 220:619–26. With J. Ashmore and G. F. Cahill, Jr. Intracellular ionic environment and enzyme activities; carbohydrate metabolism in liver. Arch. Biochem. Biophys. 65:78–85. 1957 With J. Ashmore, G. F. Cahill, Jr., and S. Zottu. Studies on carbohydrate metabolism in rat liver slices. VIII. Effects of ions and hormones on pathways of glucose-6-phosphate metabolism. J. Biol. Chem. 224:225–35. With G. F. Cahill, Jr., J. Ashmore, and S. Zottu. Studies on carbohydrate metabolism in rat liver slices. IX. Ionic and hormonal effects on phosphorylase and glycogen. J. Biol. Chem. 224:237–50. With D. Elwyn, J. Ashmore, G. F. Cahill, Jr., S. Zottu, and W. Welch. Serine metabolism in rat liver slices. J. Biol. Chem. 226:735–44. 1958 With G. F. Cahill, Jr., J. Ashmore, and S. Zottu. Studies on carbohydrate metabolism in rat liver slices. X. Factors in the regulation of pathways of glucose metabolism. J. Biol. Chem. 230:125–35. With R. G. Spiro and J. Ashmore. Studies in carbohydrate metabolism in rat liver slices. XI. Effect of prolonged insulin administration in the alloxan-diabetic animal. J. Biol. Chem. 230:751–59. With R. G. Spiro. Studies on carbohydrate metabolism in rat liver slices. XII. Sequences of metabolic events following acute insulin deprivation. J. Biol. Chem. 230:761–71. 1959 With W. C. Shoemaker, R. Mahler, J. Ashmore, and D. E. Pugh. The hepatic glucose response to insulin in the unanesthetized dog . J. Biol. Chem. 234:1631–33. 1960 With E. B. Dowdle. Effect of CO2 tension on synthesis of liver glycogen in vitro. Trans. Assoc. Am. Physicians 73:240–46. With B. R. Landau, R. Mahler, J. Ashmore, D. Elwyn, and S. Zottu.
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Biographical Memoirs: Volume 63 Cortisone and the regulation of hepatic gluconeogenesis. Endocrinology 70:47–53. With B. R. Landau, J. Ashmore, and S. Zottu. Studies on carbohydrate metabolism in rat liver slices. XV. Pyruvate and propionate metabolism and CO2 fixation in rat liver slices in vitro. J. Biol. Chem. 235:1856–58. With J. E. Richmond. Distribution of sulfate in blood and between cerebrospinal fluid and plasma in vivo. Am. J. Physiol. 199:814–20. With J. E. Richmond. Distribution equilibria of sulfate in vitro between red blood cells and plasma. Am. J. Physiol. 199:821–23. 1963 With D. D. Fanestil and T. A. Mahowald. Environmental CO2 stimulation of mitochondrial adenosine triphosphatase activity. J. Biol. Chem. 238:835–42. With B. R. Landau and S. Zottu. Substrate concentrations and metabolic pathways in liver slices in vitro. Biochim. Biophys. Acta 74:621–28. With B. R. Landau and S. Zottu. Pyocyanin and metabolic pathways in liver slices in vitro. Biochim. Biophys. Acta 74:629–34. With H. N. Christensen and B. H. Feldman. The concentrative and reversible character of intestinal amino acid transport. Am. J. Physiol. 205:255–60. 1964 With W. J. Longmore and T. A. Mahowald. Effect of environmental CO 2 and pH on glycerol metabolism by rat liver, in vitro. J. Biol. Chem. 239:1700–04. With W. J. Longmore. Glycerol metabolism in choline-deficient rats. J. Nutr. 83:103–6. With W. J. Longmore and E. S. Harrison. The effect of physiological variation in pH and CO2 concentration on acetate-1-C14 metabolism. Proc. Natl. Acad. Sci. USA 52:1040–45. 1967 With W. J. Longmore, E. S. Harrison, and H. H. Liem. Effect of CO2 and cations on fatty acid and cholesterol synthesis by liver in vitro. Am. J. Physiol. 212:221–27.
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Biographical Memoirs: Volume 63 1968 With W. J. Longmore, B. R. Landau, E. S. Baker, D. M. Lum, and H. R. Williams. Effect of pH and CO2 concentration on glucose metabolism by rat adipose tissue in vitro. Am. J. Physiol. 215:582–86. (Twenty-five further bibliographic items appeared by 1989, not, however, in the category of laboratory research.)
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