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PHILIP DURYEE McMASTER September 14,1891-March 20,1973 BY WALTHER F. GOEBEL MY FIRST ENCOUNTER with Philip McMaster was in the locker room of the squash court at the Rockefeller Institute more than fifty years ago. I had come to New York but a few weeks before as a research assistant in the laboratories of Dr. Oswald T. Avery. I was in search of exercise that day, and how well I remember the sound of the squash ball on the wooden walls of the court as I entered the locker room, and the shouting and cursing which issued from the tiny balcony above the court itself. Then, suddenly, Phil and his opponent emerged panting and laughing. He extended his hand to me and introduced him- self. My first impression was of a man small in stature, witty, and cordial: something unique for me, for I had as yet made few friends in this new and overpowering metropolis. Friends we became, and we remained so from that day forth. Philip McMaster was born at Chestnut Hill in Philadelphia on the fourteenth of September 1891. His father was John Bache Master, a distinguished historian who headed the Depart- ment of History at the University of Pennsylvania and a scholar still identified as the author of History of the People of the United States. His mother was Gertrude Stevenson of Morris- town, New Jersey. There was always a constant flow of profes- sors through the McMaster household, and because of this, Phil's academic background was assured. In this environment he was to remain throughout his long and productive life. 287
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288 BIOGRAPHICAL MEMOIRS His early education in Philadelphia was obtained in private schools, and upon his graduation he entered Princeton Univer- sity, from which he graduated in 1914. During his summers, as a boy, he accompanied his family to Kennebunkport, Maine, and to Cape Cod, where he developed his love of the outdoors and of the sea as well. These were hobbies which never left him. His early taste for biology undoubtedly arose when he accom- panied his father and Professor Edward Conklin on frequent field trips to collect biological specimens. Conklin was professor of biology at the University of Pennsylvania and spent his sum- mers at the Marine Biological Laboratory in Woods Hole. These forays were always made on bicycles, and the treasures which they collected were returned to the laboratory, where they were subjected to exhaustive scrutiny by the professor. Philip's summers in Maine were filled with water sports of every descrip- tion. At the age of nine he was given his first sailboat, a craft some fifteen feet long, of which he soon became master. After Philip graduated from Princeton in 1914 with the degree of bachelor of science, he entered the medical school of the University of Pennsylvania, where he was graduated the year World War I ended. Fortunately, McMaster was not devoted totally to scholarship during his college years, for as an under- graduate, not long after he entered Princeton, he was made coxswain of the freshmen crew a happy choice, for he and water, both fresh and salt, remained inseparable during his entire life. I am fortunate to have in my hand an account of his life and his scientific achievements ("Dr. Philip D. McMaster: His Work and Its Significance," unpublished), which he himself wrote for Dr. Herbert Gasser, the second director of the Rocke- feller Institute. Phil was the younger of two sons, the elder of whom died of pernicious anemia at the age of twenty-five. But Phil was to live beyond the allotted biblical span to pursue his distinguished scientific career, all of it at our Institute. He him-
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PHILIP DURYEE McMASTER 289 self says that during his boyhood there was but little evidence of a scholarly attitude on his part, despite the academic atmosphere in which he was raised. Personally, I doubt this. Philip served as resident physician at the medical school hospital during the last year of his medical training at the Uni- versity of Pennsylvania and again during the year following his graduation from medical school. He was commissioned as a first lieutenant in the U.S. Army shortly before the war was over. At the termination of the war and in the autumn of 1919, he came to the Rockefeller Institute as a research associate in the laboratory of Dr. Francis Peyton Rous, where he embarked upon his first investigative work. In the ensuing pages I shall attempt a resume of his more important contributions. During his first three years at the Institute, McMaster col- laborated intimately with Rous in their research. Among their achievements was the devising of methods for the intubation and sterile drainage of the gallbladders and bile ducts of a variety of animal species, a technique which permitted them to collect bile from the individual liver lobes of a number of different experimental animals and thus enabled them to com- pare them. These studies revealed that the normal gallbladder rapidly concentrates hepatic bile but that the diseased organ fails in this function. These observations were promptly utilized by clinical surgeons as a basis for diagnostic dye tests for the presence of gallstones and gallbladder disease. The basis for the test lay in the fact that in the normal organ the concentration of x-ray opaque dyes, when injected into the bloodstream, is ex- creted in the bile. This is not the case in the diseased gallbladder. As a result of these studies it became important to learn whether the liver bile of animals lacking a gallbladder is ex- creted in a form more concentrated than that of those species possessing the organ. To test this, the pigment content of bile- an index of its concentration was compared in two closely related species, namely, the mouse, which has a gallbladder, and
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290 BIOGRAPHICAL MEMOIRS the rat, which does not. Thus, the bile of rats was found to be several times more concentrated than was the bile of mice when collected by semimicro methods from individual lobes of the animals' livers. Yet when the bile of the mouse was collected from the common duct after the secretion had been acted upon by the gallbladder, the pigment content was several times greater than that of the liver bile. These studies and others on bile secretion, which extended over a period of several years, led to the development of wholly new techniques and threw new light upon the effects of diet inanition, exercise, and liver derange- ment on bile secretion. Their studies yielded, furthermore, convincing evidence that bilirubin had no other source than hemoglobin. McMaster's three years of association with Dr. Peyton Rous served well as a period of initiation for the work upon which he was next to embark with Dr. Robert Elman, namely, the pathology and physiology of urobilin. This was a problem much disputed at the time and was one of considerable importance to the understanding of the mechanism of the pigment changes in certain liver derangements, including pernicious anemia. The two men developed a procedure for collecting sterile bile, a technique which allowed them to collect the secretions either from the whole liver or from a part. Prior to this experiment. it had been thought that only the damaged liver formed urobilin, an assumption that arose as a result of finding some animals bearing infected bile fistulas. Yet, when it became possi- ble to obtain bile which remained sterile by using their intuba- tion technique, the complete loss of the secretion from the body resulted in the total disappearance of urobilin and urobilinogen from the bile, feces, and urine. This occurred when the animals were subjected to severe liver damage, biliary obstruction, or blood destruction. On the other hand, all of these led to severe urobilinuria, a condition in which bile was permitted to reach the intestines. Thus it became clear that urobilin could not be
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PHILIP DURYEE McMASTER 291 formed by the damaged liver. In brief, these experiments settled once and for all the question of the origin of urobilinuria. Thus urobilin in the urine depended first on its absorption from the intestine, or the infected biliary tract, and next upon the failure of the liver cells to remove pigment. Their findings were sub- sequently confirmed by other investigators. It was with Dr. Douglas Drury, whom I had met many years before on the first clay with McMaster in the squash court locker room, that McMaster developed the technique for the partial or total removal of the liver of experimental animals. These two men were among the first to perform hepatectomies successfully enough that the animals survived sufficiently long to enable the investigators to study the effect of liver deprivation or insufficiency upon carbohydrate and fat metabolism. This work on hepatectomized rabbits revealed that the liver was the source of blood fibrinogen. Shortly after the completion of this work, McMaster spent a sabbatical year at Harvard University, where he worked with Dr. Harry Murray in the field of psychology. Upon his return to the Rockefeller Institute he again joined Rous and his colleague Hudack in a study of the fluid interchange between the smallest blood vessels and tissues. They found that by injecting vari- colored dyes in the bloodstream of rabbits and mice, they could observe the pattern and spread of the dye's passage through the various vessel walls and changes in vascular permeability result- ing from a variety of physiological and pathological conditions such as light, trauma, heat, or cold. These experiments, to be described subsequently, were, I think, some of his finest. McMaster next turned to a study of the lymphatic system and the mechanisms of lymph flow, an investigation in which Dr. Huciack again collaborated. The two found that when bright blue vital dyes were injected into the skin of animals superficially, and more particularly into the ears of mice, they rendered the minute lymphatics visible. These experiments pro-
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292 BIOGRAPHICAL MEMOIRS vided an entirely new concept of the activities of the lymphatic system. To me, these numbered among McMaster's most interesting and rewarding experiments. How well I remember his enthu- siasm for the work as it was being executed, perhaps some four decades ago, not only on experimental animals, but upon him- self and other normal human subjects as well. These experi- ments proved that instead of being passive drainage canals, the lymphatics were very active in the process of fluid exchange. Their walls respond rapidly to various influences such as sun- light warmth or a stroke that does not break the skin. For the first time, too, these investigators were able to render the lym- phatic capillaries visible in the skin of man. When a blue dye was injected into the skin of the legs or arms, it was taken up into torn lymphatics and rendered them visible. The color appeared later as blue streamers in the draining lymphatic trunks running up the limbs. In collaboration with Dr. Robert Parsons there followed many experiments to determine the influence of the factors responsible for the movement of peripheral lymph. Both the pulsation of blood vessels as well as the mechanical effects of muscular contractions proved to be of importance. The two devised ingenious methods for measuring the pressures which existed within cutaneous lymphatic capillaries and in the in- terstitial tissues outside of them, both under normal conditions and in edematous states. They found that a gradient pressure exists between the two tissues and lymph in the capillaries suf- ficient to account for the flow of lymph in motionless skin. The structural conditions in the interstitial tissues of the skin re- vealed that fluids move along fibrillae and fibers and that open tissue spaces, filled with free fluid, such as seems to be present in sections of fixed dehydrated tissues, probably do not exist in living intradermal tissue. Instead, a gelatinous ground substance is apparently present between the formed elements.
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PHILIP DURYEE McMASTER 293 They next turned their attention to the flow of lymph under pathological conditions. By injecting dyes into the cutaneous lymphatics of edematous humans, they found differences of flow in various forms of edema. Thus, in patients with cardiac in- sufficiency and severe edema of the legs, the cutaneous lym- phatics were more dilated than in those suffering from nephrotic edema or in normal individuals. On the other hand, patients who suffered from nephrotic edema, yet who had good cardiac action, exhibited a flow of lymph more rapic! than in normal humans. It should be added that in the first group of patients, those with cardiac-insufficiency, it appeared that the lymphatic valves no longer functioned and the patients suffered from valvular incompetence of the lymphatic vessels, allowing stagna- tion of lymph in peripheral areas and even permitting retro- grade flow when slight pressure on the skin was made with the finger moving toward the foot, a fact which was not true in normal individuals. These experiments of McMaster and his younger colleagues had far-reaching consequences. Other investigators employed his techniques to study cancer patients in order to trace the lymph drainage from the diseased areas and render the lymph nodes blue, hence visible, in regions where metastases could occur through the lymph stream. McMaster's studies brought ample evidence that injury to the skin, however superficial, invariably involved the lymphatics and that local intradermal injections were, in reality, a general injection because of rapid lymphatic distribution. Every injury that breaks the continuity of the skin permits bacteria, viruses, and other foreign matter to enter the lymphatics, and because of this drainage it is not improbable that the regional lymph nodes play an important role in the defense of the body against invasion by an infectious agent. There now followed important experiments, first with Dr. Stephen Hudack and later with Dr. John Kidd, in which it Bras conclusively demonstrated that lymph nobles, draining skin sites
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294 BIOGRAPHICAL MEMOIRS injected either with bacteria or viruses, formed antibodies against these agents in very high concentrations. Confirmation of this important discovery was made in many other labora- tories. These studies were extended to ascertain the type of cells within the lymph nodes themselves and within the spleen which might be responsible for antibody formation. The clear-cut proof which McMaster's experiments presented led to a resur- gency of interest in the activities of lymphocytes. With the entrance of our country into World War II, McMaster became completely involved in wartime activities, first with the director of the Rockefeller Institute Dr. Herbert Gasserand Dr. Rene Dubos, then later with Dr. George Hoge- boom. This work was done under the auspices of the National Research Council and the Office of Scientific Research and Development and consisted of research itself as well as consulta- tion with the army and navy in an effort to devise tests for war gases and prophylactic ointments against vesicants and treatment for vesicant burns. This work consumed nearly five years of McMaster's fruitful life, and knowing him as I did, and knowing his love of fundamental research, I am not wrong when I say that during this interval there were times when he was truly frustrated. The war ended. Once again McMaster was free to return to his research and the important problems concerned with anti- body formation. In this work he made use of azoproteins colored intensely blue to study their escape through the vessel walls and to use them as tracers in order to learn about their storage and localization during antibody formation. He observed that mice previously injected and then injected a second time some weeks later suffered intense anaphylactic shock. When anesthetized animals were placed in plasteline molds with their ears spread out on a white porcelain plaque, the vascular changes and the accompanying changes in blood flow could readily be observed in the unmolested tissue of the ear. An extraordinary local and
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PHILIP DURYEE McMASTER 295 general constriction and dilation of both arterial and venous vessels occurred, yet the capillaries showed no apparent reaction. This technique using these intensely colored antigens proved extraordinarily sensitive and enabled him to follow their fate in the mammalian body. Thus, their injection into the bloocl- stream of mice revealed that the antigens were taken up both by cells of the reticuloendothelial systems throughout the body, especially the Kupffer cells of the liver, and by macrophages and reticular cells of the spleen and the lymph nodes. In this manner they revealed certain of the sites from which the first stimuli to antibody formation arose. These early studies on the sites of antibody formation in mice were considerably extended by McMaster when he next employed a much more highly diffusible blue azoprotein com- plex. When the latter was injected into the animal the complex was eliminated from the body with speed, in approximately two hours, and it was impossible to see any residual granules in the cells. Nevertheless, minute amounts of blue material, whether complete antigen or not, persisted in certain tissues of the ani- mals. In order to understand more fully the mechanism of anti- body formation, McMaster had to determine whether or not this was intact antigen or whether it was the chromophoric group which split off from the carrier protein. Without entering into detail, let me say that by means of very sensitive passive ana- phylaxis experiments McMaster showed that the antigenic mate- rial itself and not the chromophoric group of the antigen per- sisted in very small amounts in the tissues of the experimental animals. Despite these findings, it still remained possible that the persistence of the protein antigens in donor mice might exist because the animals formed antibodies very poorly; hence the antigen might indeed persist because of a lack of antibody to destroy it. The experiments were therefore repeated in rabbits, animals which are well known to be excellent antibody pro- ducers. In these experiments, McMaster employed bovine
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296 BIOGRAPHICAL MEMOIRS gamma globulin as the antigen. The results were in essence the same. By following the fate of the tracer antigen, McMaster and his co-workers next attempted to study the mechanism of antibody formation under various conditions. Since the first step in the formation of an antibody appears to be the capture of the anti- gen by phagocytic cells or even other cellular types, it seemed likely that something might be learned by observing the fate of the tracer antigen in mice which had been stimulated to form antibodies but prevented from doing so by large doses of corti- sone. Although the drug reduced the size of the lymph nodes and spleen by some ninety percent, it was observed that the shriveled organs took up as much of the tracer as did organs of normal mice, thus demonstrating unequivocally that the inhibi- tion of antibody formation did not result from the faulty uptake of antigen. Nor did it result from an impairment of the anti- genicity of the antigen or from a more rapid destruction than that which occurs in animals given no cortisone. Mice injected with foreign protein were prevented from forming antibodies by the administration of cortisone for nearly two weeks, yet upon withdrawal of the drug, antibodies promptly appeared. Clearly, the antigen had remained in the organs of the mice in a form capable of engendering antibodies. Cortisone did not inhibit antibody formation by interfering with the storage or distribution of the tracer antigen or by destroying it. The phagocytic cells, even under the influence of cortisone, continued to localize and store the tracer antigen. The undisturbed function of these cells suggests that they do not form antibodies, although they partake of the first step in antibody formation by capturing and holding the antigen. It is the cells of the lymphoid series, though greatly injured and reduced in number by cortisone, which appear to be the units which form the antibody. At about this time there appeared accounts in the literature
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PHILIP DURYEE McMASTER 299 however, I recall when his judgment was not good. It was when he asked me and two of my colleagues to sail his yacht from Huntington, Long Island to Woods Hole. Only one of us, Tom Hughes, who was then associated with the Rockefeller Founda- tion, knew anything at all about sailing and navigation. But under Hughes' short and forceful tutoring we made it, by good navigation, luck, and some dead reckoning, for we were en- gulfed in a heavy fog the entire distance. His widow, Elizabeth, whom I also know well, has permitted me to read several personal letters which she received over the past fifty years from her husband, and from these I have gotten certain impressions that I otherwise would not have had, despite the fact that we were friends of many years standing. At home, he was a charming host. He frequently entertained guests with his violin or his accordion, both of which he played with equal facility. His dress was at times a bit bizarre, for I saw him frequently on his way to the Rockefeller Institute, particu- larly in a snowstorm, dressed in the garb of a Maine woodsman, unconventional, to say the least, in the city of New York. His relationship to his wife was one of deepest affection, as attested to by two very personal letters which Elizabeth permitted me to read. They were written during World War II, when he was stationed in Florida. These letters also served to express his opinion of the shortcomings of military red tape. I have at hand, too, several letters written to Mrs. McMaster, in which the writers refer to Dr. McMaster and his work. I wish to quote from two of these, for they are from men of distinction in their own right. Dr. Merrill Chase of our Institute, in a letter to Elizabeth, says, "I look back over the years to Phil's exciting work in tracing the lymphatics of the human skin and in animals too. He was a highly ingenious research worker and I learned much from him." Then again in a telegram of condolence, James and Margaret German say, "We send love to you and our deepest sympathy. We will miss Phil because he was one of those few who showed that it was good to be human and alive."
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300 BIOGRAPHICAL MEMOIRS BIB LI O GRAPHY 1919 The germicidal power of antiseptic oils and of substances dissolved in oil. l. Infect. Dis., 24:378. 1920 With P. Rous. Vicious activity of the gall bladder during biliary stasis. Proc. Soc. Exp. Biol. Med., 17: 159. With P. Rous. The determining factor in the causation of white stasis bile. Proc. Soc. Exp. Biol. Med., 17: 159. With P. Rous. The concentrating activity of the gall bladder. Proc. Soc. Exp. Biol. Med., 17:215. 1921 With P. Rous. The biliary obstruction required to produce jaundice. J. Exp. Med., 33:731. With P. Rous. The concentrating activity of the gall bladder. l. Exp. Med., 34:47. With P. Rous. Physiological causes for the varied character of stasis bile. J. Exp. Med., 34:75. With H. Haessler. The factor determining the spread of red marrow during anemia. J. Exp. Med., 34:579. 1922 Do species lacking a gall bladder possess its functional equivalent? J. Exp. Med., 35: 127. With P. Rous and G. O. Broun. The experimental production of gallstones in dogs, in the absence of infection, stasis, and gall bladder influence upon the bile. Proc. Soc. Exp. Biol. Med., 20:128. With P. Rous and L. C. Larimore. Significance of the hemosiderosis of pernicious anemia. J. Exp. Med., 35:521. 1923 The significance of the gall bladder. Proc. Am. Philos. Soc., 62:185. With P. Rous. A method for the permanent sterile drainage of intra-abdominal ducts, as applied to the common duct. l. Exp. Med., 37:11. With G. O. Broun and P. Rous. Studies on the total bile. I. The
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PHILIP DURYEE McMASTER 301 effect of operation, exercise, hot weather, relief of obstruction, intercurrent disease, and other normal and pathological in- fluences. l. Exp. Med., 37: 395. With P. Rous and G. O. Broun. Studies on the total bile. II. The relationship of carbohydrates to the output of bile pigment. J.Exp.Med.,37:421. With P. Rous. Hydrohepatosis, a condition analogous to hydrone- phrosis. Proc. Nat. Acad. Sci., 9:19. With P. Rous and D. R. Drury. The genesis of gall stones in the dog. Proc. Soc. Exp. Biol. Med., 20:315. With G. O. Broun and P. Rous. Studies on the total bile. III. On the bile changes caused by a pressure obstacle to secretion; and on hydrohepatosis. l. Exp. Med., 37: 685. With G. O. Broun and P. Rous. Studies on the total bile. IV. The enterohepatic circulation of bile pigment. l. Exp. Med., 37:699. With G. O. Broun and P. Rous. Studies on the total bile. V. The relation between blood destruction and the output of bile pig- ment. l. Exp. Med., 37:733. 1924 With P. Rous. The liver requirement of the fasting organism. l. Exp. Med., 39:425. With P. Rous and D. R. Drury. Observations on some causes of gall stone formation. I. Experimental cholelithiasis in the absence of stasis, infection and gall bladder influence. l. Exp. Med., 39:77. With P. Rous and D. R. Drury. Observations on some causes of gall stone formation. II. On certain special nuclei of deposition in experimental cholelithiasis. l. Exp. Med., 39:97. With D. R. Drury and P. Rous. Observations on some causes of gall stone formation. III. The relation of the reaction of the bile to experimental cholelithiasis. l. Exp. Med., 39:403. Studies on the total bile. VI. The influence of diet upon the output of cholesterol in the bile. J. Exp. Med., 40:25. 1925 With R. Elman. Studies on urobilin physiology and pathology. I. The quantitative determination of urobilin. J. Exp. Med., 41:503. With R. Elman. Studies on urobilin physiology and pathology. II. Derivation of urobilin. Relation of the bile to the presence of urobilin in the body. J. Exp. Med., 41:513.
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302 BIOGRAPHICAL MEMOIRS With R. Elman. Studies on urobilin physiology and pathology. III. Absorption of pigments of biliary derivation from the intestine. J. Exp. Med., 41:719. With R. Elman. Studies on urobilin physiology and pathology. IV. Urobilin and the damaged liver. l. Exp. Med., 42:99. \Vith R. Elman. Studies on urobilin physiology and pathology. V. The relation between urobilin and conditions involving increas- ing red cell destruction. l. Exp. Med., 42:619. 1926 With R. Elman. Studies on urobilin physiology and pathology. VI. The relation of biliary infections to the genesis and excretion of urobilin. l. Exp. Med., 43: 753. With R. Elman. The physiological variations in resistance to bile flow to the intestine. l. Exp. Med., 44:151. With R. Elman. On the expulsion of bile by the gall bladder and a reciprocal relationship with the sphincter activity. l. Exp. Med., 44:173. 1928 With D. R. Drury. Relation of liver to fat metabolism. I. Respira- tory quotient in conditions of liver insufficiency. Proc. Soc. Exp. Biol. Med., 25:151. With R. Elman and D. R. Drury. The relative reaction within living mammalian tissues. X. Litmus constituents as vital stains; their preparation and relative usefulness. l. Exp. Med., 47:777. With R. Elman. The relative reaction within living mammalian tissues. XI. The intracellular reaction of the kidney epithelium andits relation to the reaction of the urine. l. Exp. Med., 47:797. 1929 With D. R. Drury. The source of fibrinogen. Proc. Soc. Exp. Biol. Med., 26:490. With D. R. Drury. The production of partial liver insufficiency in rabbits. J. Exp. Med., 49:745. With D. R. Drury. The relation of the liver to fat metabolism. I. Effect of liver lack on fat combustion and the respiratory quotient. J. Exp. Med., 49: 765.
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PHILIP DURYEE McMASTER 303 With D. R. Drury. The liver as a source of fibrinogen. l. Exp. Med., 50:569. 1930 With D. R. Drury. Irreversible character of the late changes after hepatectomy. Proc. Soc. Fop. Biol. Med., 27:47. With D. R. Drury. Glucose requirement of hepatectomized rabbits and its relation to lactic acid production. Proc. Soc. Exp. Biol. Med., 27:48. 1931 With S. S. Hudack. The permeability of the lymphatic wall. Proc. Soc. Exp. Biol. Med., 28:852. With S. S. Hudack. The breakdown of lymph transport. Proc. Soc. Exp. Biol. Med., 28:853. 1932 With S. S. Hudack and P. Rous. The relation of hydrostatic prep sure to the gradient of capillary permeability. J. Exp. Med., 55:203. With S. S. Hudack. Vessels involved in hydrostatic transudation. I. Exp. Med., b5:417. With S. S. Hudack. The gradient of permeability of the skin vessels as influenced by heat, cold, and light. J. Exp. Med., b5:431. With S. S. Hudack. Normal and pathological permeability of the lymphatic capillaries in human skin. Proc. Soc. Exp. Biol. Med., 29:944. With S. S. Hudack. I. The permeability of the wall of the lymphatic capillary. J. Exp. Med., 56:223. With S. S. Hudack. II. Induced alterations in the permeability of the lymphatic capillary. J. Exp. Med., 56:239. 1933 With S. S. Hudack. The lymphatic participation in human cutane- ous phenomena; a study of the minute lymphatics of the living skin. l. Exp. Med., 57:751. With P. Rous and S. S. Hudack. The fixation of certain viruses on the cells of susceptible animals and the protection afforded by such cells. Proc. Soc. Exp. Biol. Med., 31:90.
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304 BIOGRAPHICAL MEMOIRS 1934 With S. S. Hudack. Formation of agglutinins within lymph nodes. Proc. Soc. Exp. Biol. Med., 31:751. With S. S. Hudack. Agglutinin formation within the lymph nodes of resistant and susceptible mice. Proc. Soc. Exp. Biol. Med., 31:753. With S. S. Hudack. The participation of skin lymphatics in repair of the lesions due to incisions and burns. T. Exp. Med., 60:479. With D. R. Drury. Irreversible character of the late changes after hepatectomy. J. Exp. Med., 60:503. 1935 With P. Rous and S. S. Hudack. The fixation and protection of viruses by the cells of susceptible animals. l. Exp. Med., 61:657. Rate of lymph flow in edematous skin of cardiac and renal disease. Proc. Soc. Exp. Biol. Med., 32:1178. With S. S. Hudack. The formation of agglutinins within lymph nodes. l. Exp. Med., 61: 783. 1936 With I. G. Kidd. Development of antiviral properties within lymph nodes. Proc. Soc. Exp. Biol. Med., 34:547. 1937 Changes in the cutaneous lymphatics of human beings and in the lymph flow under normal and pathological conditions. J. Exp. Med., 65:347. The lymphatics and lymph flow in the edematous skin of human beings with cardiac and renal disease. l. Exp. Med., 65:373. With J. Go Kidd. Lymph nodes as a source of neutralizing principle for vaccinia. l. Exp. Med., 66:73. 1938 With R. l. Parsons. Path of escape of vital dyes from the lymphatics into the tissues. Proc. Soc. Exp. Biol. Med., 37:707. With R. l. Parsons. Effect of the pulse on lymph formation and interstitial movement of substances. Proc. Soc. Exp. Biol. Med., 38:408.
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PHILIP DURYEE McMASTER 305 With R. J. Parsons. The effect of the pulse upon the formation and flow of lymph. J. Exp. Med., 68:353. With R. I. Parsons. The effect of the pulse on the spread of sub- stances through tissues. A. Exp. Med., 68:377. With R. I. Parsons. Normal and pathological factors influencing the spread of a vital dye in the connective tissue. l. Exp. Med., 68:869. 1939 With R. J. Parsons. Physiological conditions existing in connective tissue. I. The method of interstitial spread of vital dyes. i. Exp. Med., 69:247. With R. l. Parsons. Physiological conditions existing in connective tissue. II. The state of the fluid in the intradermal tissue. I. Exp. Med., 69:265. 1941 Intermittent take-up of fluid from the cutaneous tissue. I. Exp. Med., 73:67. Factors influencing the intermittent passage of Locke's solution into living skin. J. Exp. Med., 73:85. An inquiry into the structural conditions affecting fluid transport in the interstitial tissue of the skin. l. Exp. Med., 74:9. A method to determine the peripheral arterial blood pressure in the mouse. l. Exp. Med., 74:29. 1942 Lymphatic participation in cutaneous phenomena. Harvey Lec- tures, 37:227. 1943 The lymphatic system. Annul Rev. PhysioI., 5:207. 1945 With G. H. Hogeboom. The development of methods for testing the abilities of agents to combat the effects of mustard gas, H. and other vesicants upon the skin. Office of Scientific Research and Development, National Defense Research Comm., Div. 9 Rep. No. 4853.
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306 BIOGRAPHICAL MEMOIRS With G. H. Hogeboom. A search for decontaminating and treat- ment agents for skin exposed to mustard gas, H. Once of Scientific Research and Development, National Defense Research Comm., Div. 9 Rep. No. 4854. With G. H. Hogeboom. The necrotizing action of certain sub- stances related to mustard gas, H. or the nitrogen mustards. Once of Scientific Research and Development, National Defense Research Comm., Div. 9 Rep. No. 4852. With G. H. Hogeboom. A comparison of the vesicant action exerted upon human skin by mustard gas, H. and by mixtures of H with wetting agents or solvents. Once of Scientific Research and Development, National Defense Research Comm., Div. 9 Rep. No. 4852. With G. H. Hogeboom. The inhibition of Gesticulation in mustard gas, H. lesions of human skin by BAL. Office of Scientific Research and Developments, National Defense Research Comm., Div. 9 Rep. No. 5027. With G. H. Hogeboom. Changes in the circulation and in the permeability of vessels within and about mustard gas and Lewisite lesions of rabbit skin. Office of Scientific Research and Development, National Defense Research Comm., Div. 9 Rep. No. 5026. 1946 introduction: Lymph. A conference held at the New York Academy of Sciences. Ann. N.Y. Acad. Sci., 46:679. Conditions in the skin influencing interstitial fluid movement, lymph formation and lymph flow. Ann. N.Y. Acad. Sci., 46:743. The pressure and interstitial resistance prevailing in the normal and edematous skin of animals and man. l. Exp. Med., 84:473 The effects of venous obstruction upon interstitial pressure in animal and human skin. J. Exp. Med., 84:495. 1947 The relative pressures within cutaneous lymphatic capillaries and the tissues. J. Exp. Med., 86:293. 1949 With H. Kruse. Peripheral vascular reactions in anaphylaxis of the mouse. J. Exp. Med., 89:583.
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PHILIP DURYEE McMASTER 307 With H. Kruse. The distribution and storage of blue antigenic azoproteins in the tissues of mice. l. Exp. Med., 90:425. 1950 With H. Kruse. Persistence of antigen. Fed. Proc. 9:387. With R. I. Parsons. The movement of substances and the state of the fluid in the intradermal tissue. Ann. N.Y. Acad. Sci., 52:992. 1951 With H. Kruse. The persistence in mice of certain foreign proteins and azoprotein tracer antigens derived from them. J. Exp. Med., 94:323. With H. Kruse. The behavior and persistence of azoprotein tracer antigens in mice. Fed. Proc., 10:564. 1953 The sites of antibody formation. In: The Nature and Significance of the Antibody Response, ed. A. M. Pappenheimer, pp. 13~. N.Y.: Columbia Univ. Press. 1954 With H. Kruse, E. Sturm, and i. L. Edwards. The persistence of bovine >-globulin injected as an antigen into rabbits. A com- parison with its previously studied persistence in mice. J. Exp. Med., 100:341. With H. Kruse, E. Sturm, and I. L. Edwards. Persistence of antigen in rabbits contrasted with that in mice. Fed. Proc., 13:505. 1955 With l. L. Edwards and E. Sturm. Active anaphylaxis to a foreign protein induced in mice by the transfer of tissue from animals previously injected with the protein. l. Exp. Med., 102:119. 1957 With l. L. Edwards. Impairment of the antigenicity of a protein antigen following its injection into rabbits. J. Exp. Med., 106: 219. With i. L. Edwards. The behavior of two foreign protein antigens in mice during inhibition of antibody formation by cortisone. Proc. Nat. Acad. Sci., 43:380.
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308 BIOGRAPHICAL MEMOIRS 1959 General and local vascular reactions in certain states of hypersensi- tivity. A limited review of previous work. In: Cellular and Humoral Aspects of the Hypersensitive States, ed. H. S. Lawrence, pp. 319-353. N.Y.: Paul B. Hoeber. 1960 With M. Heidelberger. Florence Rena Sabin. In: Biographical Memoirs, 34:271-319. Wash., D.C.: National Academy of rot . sciences. 1961 Antibody formation. In: The Cell, eds. I. Bracket and A. E. Mirsky, pp. 323-404. N.Y.: Academic Press. With R. E. Franzl. The effects of adrenal cortical steroids upon antibody formation. Metabolism, 10:990. \Vith R. E. Franzl. Effect of bacterial lipopolysaccharides on hemo- lysin formation in mice. Fed. Proc., 20:26. 1968 'with R. E. Franzl. The primary immune response in mice. I. The enhancement and suppression of hemolysin production by a bacterial endotoxin. l. Exp. Med., 127:1087. \Vith R. E. Franzl. The primary immune response in mice. II. Cellular responses of lymphoid tissue accompanying the en- hancement or complete suppression of antibody formation by a bacterial endotoxin. l. Exp. Med., 127: 1109. 1971 Peyton Rous. N.Y.: The Rockefeller Univ. Press. 13 pp.
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Representative terms from entire chapter: