Boston City Hospital Research Articles

Hepatic Wilson’s disease: Initial treatment and long-term management

This article is based on the experience of 320 patients with Wilson's disease who were seen between the years 1954 and 2000. These patients were seen at The Boston City Hospital, 1954 thru 1955, University College Hospital, London,1955 thru 1957; Addenbrooke's Hospital, Cambridge, 1967 thru 1987, and The Middlesex Hospital London, 1988 thru 2000. Wilson's disease is not strictly a gastroenterologic disease but a genetically determined metabolic disease that is mediated by a failure of copper excretion through the bile. The mutation carried on chromosome 13q14.3: it involves a copper-carrying ATPase (ATPase 7B); more than 250 mutations are now known. The first organ to be affected is the liver, then many other tissues, principally the brain but also the eyes, the kidneys, the bone marrow, and the osteoskeletal system. It is with the hepatic form of the disease that this article is concerned. The hepatic illness may be acute, subacute or chronic; it may be progressive or, apparently, self-limiting. In 10% of patients hemolysis may also be found which can later lead to the formation of pigment gallstones. The management of liver disease is not considered in this article, which is strictly confined to the therapeutic options available for the elimination of copper and the long-term welfare of the patient. It must be remembered that all close relatives of the patient must be screened for the presymptomatic stage of the disease so, if they are found to be homozygous carriers for the mutation, they can be started on preventive treatment.

Judah Folkman: persistent pioneer in cancer research

Judah Folkman: persistent pioneer in cancer research

Sidney Carter, MD (1912–2005)

![][1] Figure. Sidney Carter, MD Dr. Sidney Carter, one of the most eminent and beloved of neurologists and a founder of child neurology, died on Sunday, January 16th, on Cape Cod. He was 92 years old. Dr. Carter was born in Boston and attended Dartmouth College. He received his medical degree from Boston University in 1938. He interned at St. Mary’s Hospital in Waterbury, CT and then trained in psychiatry in 1939 to 1940 at the Westboro State Hospital in Westboro, MA. In 1941, he started his residency in neurology on the Harvard Unit at Boston City Hospital, where Houston Merritt had recently been appointed Acting Director, following the departure of Tracy Putnam to the Neurologic Institute of New York. In addition to Merritt, Carter worked closely with Raymond Adams, then also at the Boston City Hospital. In 1943, Derek Denny-Brown was named Director of the Neurology Service and, 2 years later, Merritt left to direct Columbia’s neurology program at Montefiore Hospital in the Bronx. Carter had the distinction of being Merritt’s last chief resident at Boston City, and Denny-Brown’s first. During World War II, Carter joined other physicians from the Boston City Hospital at the Seventh General Army Hospital in England, where he was assistant chief of the neuropsychiatric section and the principal neurologic consultant for army casualties. His military career had … [1]: /embed/graphic-1.gif

Neurology of Learning Disabilities: What Will the Future Bring? The Answer Comes from the Successes of the Recent Past

My involvement with learning disabilities (LD) began approximately 25 years ago, at a time when formal research training was uncommon for medical doctors, and the apprenticeship model was the way most of us began our research careers. Of all the topics I had heard Norman Geschwind--at that time my neurology chairman and mentor--speak about, language held particular fascination for me, perhaps because of my own experience with having to learn and become competitive in a new language at age 15. After completing my residency, I began to work on anatomic brain asymmetries in an attempt to further understand the biological specialization of the left hemisphere for many aspects of language function. Then, Geschwind invited Friedrich Sanides, a late student of Oskar and Cecile Vogt (Brodmann was an earlier student), to travel to Boston from West Germany and spend a year here teaching me about cytoarchitectonics as a neuroanatomical tool to deepen the study of brain asymmetries. This took place in 1977. In 1978, Geschwind suggested that I take over a project begun by Dr. Brooke Seckel, a resident two years my senior, who had decided to change careers (I often wondered whether it was the project that did it). It concerned the study of a brain from an individual with developmental dyslexia who had died as a result of a fall down an elevator shaft. His brain had become part of the Yakovlev Collection at the Boston City Hospital, where all of this took place. Brooke had been testing the hypothesis, advanced by Geschwind, that the brain of a dyslexic would show two small plana temporale. In 1968 Geschwind and his then student Walter Levitsky had shown in the general population that the planum temporale, comprising part of the auditory association cortex involved in linguistic functions, was large on the left and small on the right, perhaps explaining language lateralization to the left hemisphere. Some normal brains showed the reverse asymmetry, and still others showed lack of asymmetry, with a large planum on both sides. It made sense to Geschwind, a believer in the phrenological principles that had been launched at the start of the nineteenth century, that in a condition with poor language function, the plana would be bilaterally small (in one interpretation of phrenology, more brain tissue means more function). Here is where I became involved. As it turned out, the plana temporale were not small in the dyslexic brain, but were shown to be large in several specimens of dyslexic brains; later, additional alterations in planum asymmetry were reported. Animal experiments showed that under some conditions symmetry in a cortical area could be a response to a disorder of neuronal migration. In fact, the first dyslexic brain and many other brains showed cortical dysplasias and ectopias resulting from abnormal neuronal migration to the cerebral cortex during mid-gestation. This finding began a productive area of research that lasted the better part of two decades. Initially, it was important to establish that these focal cortical malformations significantly disrupted cortico-cortical organization and cortico-thalamic interactions, to explain linguistic deficits, which was done after it was possible to model the anomalies in experimental rodent models. Second, it was necessary to show that the cortical malformations and the cortico-thalamic anomalies produced (and were not simply correlated with) functional deficits. Thus, it was shown that induction of cortical malformations in the rat, similar to those found in the dyslexic brain, produced a variety of cognitive deficits, and that disturbances in cortico-thalamic networks were associated with perceptual deficits involving processing of rapidly changing sound stimuli. Thus, a causal interaction was established between focal disorders of neuronal migration and some behaviors that mimicked deficits found in populations of dyslexic individuals. A second focus of research concerned the origin of the cortical and thalamic malformations in the dyslexic brain. …

A Vision for the Future

A Vision for the Future

Denny-Brown, Boston City Hospital, and the history of American neurology.

Harvard University's Neurological Unit at Boston City Hospital (BCH) became the premier center for neurological training in the United States during the middle part of the 20th century. During part of this period (1939-1967), it was directed by Derek Denny-Brown, who had been recruited from England by Harvard president James Conant. The training program that Denny-Brown initiated at BCH emphasized neurology as a medical specialty, independent of psychiatry and neurosurgery. This program, which reflected Denny-Brown's British training, was remarkably effective and served as a model for rest of the country.

Response:

Response:

Public Sector Unions Shaping Hospital Privatization: The Creation of Boston Medical Center

In this paper the author examines, through a case study of a hospital merger in Boston, MA, the ways in which a locally scaled union strategy can shape privatization. She first examines recent economic changes in the US hospital industry, which have resulted in a record number of mergers, closures, and conversions. A case study of the merger between a public hospital, Boston City Hospital, and a private hospital, Boston University Hospital, into the private, nonprofit, Boston Medical Center is presented to demonstrate the ways in which unions can participate in setting the terms of such mergers. The strategy of one labor union local in particular, the Service Employees International Union (SEIU) Local 285, is examined in regard to protecting both the provision of public healthcare and the conditions of employment during and after the process of privatization. By utilizing a local strategy and waging a highly public campaign, leaders of SEIU Local 285 were able to build coalitions with other labor unions and public healthcare advocates and played an instrumental role in setting the terms of the merger. As a result, the final merger agreement contained significant protection for quality public healthcare and labor practices favorable for workers. Unions that previously represented public sector workers now represent private sector workers, and wages for all employees moved upward as part of the agreement. In addition, the new private sector entity was charged with what had formerly been a public sector mission. In effect, although the public hospital was ultimately privatized, the private sector was restructured by local level, public sector union activism.

Neurogenic Bladder: Past, Present, and Future

Summary: The foundation of the management of neuragenie bladder can be attributed to a pioneer in spinal cord injury medicine. Dr. Donald Munro, a neurosurgeon, who also had experience in urologic surgery, established the firstSpinal Cord lnjury Service of 1 0 beds in the Boston Cityhospital in the 1 930s. He later became adviser to the US Army and the Veterans Administration (VA). On his recommendation, paraplegic centers were created in US army hospitals and later in the VA hospitals from 1 943 to 1945. This article reviews the evolution of the management of neuragenie bladder in patients with spinal cord injuries from the past century to the present. The role of urodynamics in defining neurologic lesions is critical to the appropriate management of the voiding dysfunction. Key advances, such as the diagnosis of detrusor sphincter dyssynergia (DSD), recognition of its association with autonomic dysreflexia, and its definitive management, have been emphasized. The role of transrectallinear array sonography using a rectal probe was found useful for defining bladder outlet dysfunction du ring urodynamics. lt also helped to recognize secondary bladder neck obstruction and diagnose false passages in the urethra. Clean technique intermittent catheterization (IC) was evaluated and recommended. ln about 28'7'o patients with DSD that led to secondary bladder neck obstruction, a consequence of IC was reported. Transurethrallaser sphincterotomy (TURS) was first reported by mein 1 991, and later, durable 7 -yearfollow-up results were reported in 78'7'o of the first 99 patients. We reported a surgical technique to lengthen the penis. We also reported the long-term success with semirigid implants in 92'7'o of patients with SCI. This technique helped maintain external condom drainage on a small phallus and improved the sex life of patients, as weil as their quality of life. The author's pertinent areas of interest in the past one-half century were aimed at recognizing specific urologic problems associated with neurologic impairment. Management was aimed at preventive care, early recognition, and timely management to reduce secondary complications and enhance quality of life.

William Bosworth Castle: pioneer of haematological clinical investigation.

William Bosworth Castle (1897-1990) spent his entire haematological career at the Harvard Medical Unit and Thorndike Memorial Laboratory at Boston City Hospital during the golden age of haematology. Castle's experiments in solving the puzzle of pernicious anaemia by identifying the intrinsic factor are models of clinical investigation and marked a new era in haematology. Castle's insatiable curiosity about the mechanisms of disease, his ability to design and conduct simple experiments to test hypotheses, and his ability to attract clinical investigators to the Thorndike Laboratory, and inspire them and make them feel like intellectual equals, fuelled the dramatic output of seminal work on nutritional anaemias, haemolysis, splenic function, haemoglobin physiology and coagulation. Indeed it was Castle's breadth of scientific achievements in haematology and his leadership of the Thorndike Memorial Laboratory that contributed to the notion that modern haematology was born in Boston but nurtured at the Thorndike Memorial Laboratory.

Boston City Hospital and the Thorndike Memorial Laboratory: the birth of modern haematology.

Established in 1923, the Thorndike Memorial Laboratory at Boston City Hospital was the first clinical research laboratory in a municipal hospital in the United States of America. Minot and Castle, who were the second and third directors of the Laboratory, were pioneer haematologists and clinical investigators of the highest calibre who created an atmosphere at the Laboratory that would foster patient-centred research and attract the best physician-scientists to work and train there. The haematology research division of the Laboratory made important original contributions to the understanding of the pathophysiology of anaemia, the mechanisms of red cell and platelet destruction and the phagocytic role of the spleen, the nature of haemoglobin (normal and sickle cell), the nature of haemophilia and its therapy and the early classification of lymphoma. It contributed to the Thorndike Memorial Laboratory's worldwide reputation as a model research laboratory and established its reputation as the birthplace of modern haematology.

Epilogue: A Journey with Blood Cells and Viruses

THE FOCUS OF THIS JOURNAL, stem cells, strictly speaking is a subject on which I have neither published nor (unless unwittingly) worked on. Thus, although I feel both honored and grateful, nonetheless I also feel a little awkward to be featured in this Journal. Yet, oddly and quite by accident, I find myself at this very time becoming a new student of this topic, a point to which I will return at the end of this article. My first and continuous interest in research has been in the biology of blood cells—ones you could tell were really blood cells and not the phantom earliest progenitors. This interest began as a medical student at Jefferson Medical School, Philadelphia, in 1960, working in the laboratory of Alan Erslev, who was likely the first person to show in a laboratory setting the regulation of blood cell production by a human factor. Indeed, it might be justifiably stated that he was the discoverer of erythropoietin. We worked together on the impaired erythropoietic response in chronic lung disease (1). Alan advised me to head to either the Boston City Hospital or the University of Chicago for my internship and residency in medicine because these were “The centers of excellence in blood cell biology,” and I jumped at the suggestion. This notion was a bit naive because interns and residents did not then (and I assume now) have so much free time for research. I arrived in Chicago in July of 1963 and spent the next few years there. Despite the demands on the “house officers,” I could not fail to be moved by the presence of Leon Jacobson, a leader in the field of radiation-induced impairment of hematopoiesis, an erythropoietin expert, and Chairman of the Department of Medicine; Cliff Gurney, who seemed to have insights into every angle of blood cell biology; Stanley Yarcoan, a biochemist-physiologist of blood cells; Gerry Mendel, an iron-metabolism-erythropoiesis expert; and Gene Goldwasser, the first to purify erythropoietin (Epo) and to obtain its structural information. (Keep in mind that Epo was the first humoral factor to be described, purified, and analyzed for any blood cell, and among the first defined growth factors of any kind.) Then there was the indomitable Rudi Schmid, who had just arrived from the Thorndike Laboratories of Harvard’s Boston City Hospital, and was one reason why Erslev finally emphasized Chicago for me. Rudi’s interests, however, were more on the catabolic products of heme. One could hardly be surrounded by a greater collection of individuals involved in areas of research I wished to study. Cliff Gurney was also a generous man with a strong inclination to mentor. He opened his laboratory to me and fostered my independence. Consequently, despite the rigors of an internship and residency in medicine, I was able to produce a solo-authored paper on the regulation of heme biosynthesis due to Cliff Gurney (2). This was the time of the Viet Nam war. Many M.D.’s wished to avoid the draft and head to the National Institutes of Health (NIH) as research or clinical associates. Some of us wanted to go to NIH anyway because it was a place for M.D.’s to acquire the technical skills that seemed to be embedded in the character of Ph.D.’s but not of us. In those days it was strongly believed that “academically” oriented M.D.’s “had ” to go to NIH for a period. After all, that was the way of the current and past generation, and that was basically true. That is no longer true, perhaps due to a decline in the number of M.D.’s in the United States that are enamored with this kind of career, the increased opportunities in biotechnology companies, and the fact that NIH created its own competition by helping to develop so many centers of excellence in diverse areas of biomedical research throughout the country. But in 1965, NIH was the place for us.

Asymptomatic Infections of the Urinary Tract *

No AccessJournal of UrologyCLINICAL UROLOGY: Milestone in Urology1 Aug 2002Asymptomatic Infections of the Urinary Tract* Edward H. Kass, and Maxwell Finland Edward H. KassEdward H. Kass More articles by this author , and Maxwell FinlandMaxwell Finland More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(05)64650-2AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail References 1 : Factors in the pathogenesis of pyelonephritis Yale. J. Biol. & Med1955; 28: 81. Google Scholar 2 : Chemotherapeutic and antibiotic drugs in the management of infections of the urinary tract. Am. J. Med1955; 18: 764. Google Scholar 3 : The differential diagnosis of Bright’s disease: clinicopathological correlation New England J. Med1943; 229: 387. Google Scholar 4 : Antibacterial management of urinary tract infections. J.A.M.A1952; 148: 165. Google Scholar 5 : Pyelonephritis. Correlation of clinical and pathologic observations in the antibiotic era M. Clin. North America1955; 39: 297. Google Scholar 6 : Evaluation of “positive” urine culture. An approach to the differentiation of significant bacteria from contaminants. Am. J. Med1956; 20: 88. Google Scholar BOSTON, MASS.(From the Thorndike Memorial Laboratory and Second and Fourth (Harvard) Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School)© 2002 by American Urological Association, Inc.FiguresReferencesRelatedDetails Volume 168Issue 2August 2002Page: 420-424 Advertisement Copyright & Permissions© 2002 by American Urological Association, Inc.MetricsAuthor Information Edward H. Kass More articles by this author Maxwell Finland More articles by this author Expand All Advertisement PDF DownloadLoading ...

The clinical applications of EEG: origins

The first paper in our series Classics in Epilepsy and Behavior is ‘‘Epilepsy: A Paroxysmal Cerebral Dysrhythmia,’’ published in Brain by Gibbs, Gibbs, and Lennox in 1937. The paper serves as a landmark for spurring interest in the role of EEG in clinical epilepsy as well as linking the term ‘‘psychomotor epilepsy’’ to a specific EEG pattern. The application of EEG technology to human seizure disorders was slow. Richard Caton (1842–1926), a British physician, published his findings of the electrical phenomena of the exposed cerebral hemispheres of rabbits and monkeys in 1875. According to Brazier, the discovery of the EEG went unnoticed by clinicians in Western Europe and America for nearly 60 years [1]. However, work proceeded in Eastern Europe with the ‘‘rediscovery’’ of EEG by Adolf Beck (1863–1942) in Krakow, Poland, in 1891 and the tests of whether an epileptic attack might be accompanied by abnormal EEG activity in dogs by Pavel Yurevich Kaufman (1877–1951) in St. Petersburg in 1912. Gibbs, Gibbs, and Lennox thank ‘‘the pioneer work of Berger’’ in developing the EEG [2]. Indeed, Hans Berger (1873–1941), a German neuropsychiatrist, began study of the human EEG in 1924 in patients with large skull defects (post-World War I injuries), but soon recognized that readings could be made just as well through an intact skull and scalp [3]. A complex character, Berger worked in isolation with incredibly primitive equipment. The first report of 1929 recorded from the head of Berger s son featured the alpha rhythm and the alpha blocking response [4]. Berger s findings were greeted with universal skepticism, but they were eventually confirmed in 1934 by Adrian and Matthews in England [5]. While documenting the first recordings of the EEG in epilepsy, Berger failed to recognize the clinical significance of EEG to seizure disorders. Brazier explains this oversight as counter to Berger s conception of EEG as a means to study the nature of mental energy (‘‘psychische Energie’’) [1]. More a ‘‘psychophysiologist’’ than a neurophysiologist, Berger sought the correlate of mental energy in EEG. Formidable technological gaps contributed to the slow incorporation of EEG to human seizure disorders; however, conceptual gaps regarding the nature and interpretation of brain waves remained even more significant obstacles. America played no role in the early development of experimental EEG [3]. Instead, a small group of American neurophysiologists of the late 1920s deemed themselves ‘‘axonologists’’ and focused their efforts on separating the components of conducted action potentials in somatic and autonomic nerves [6]. As Gibbs recalled in an interview, ‘‘the axonologists whittled the nervous system down to one axon and knocked themselves out studying that. They told me that studying the whole brain (i.e., EEG) was just ridiculous’’ [7]. Hallowell Davis (1896–1992) and colleagues at Harvard Medical School confirmed Berger s alpha rhythm in late 1934 [8]. This demonstration lured Frederic and Erna Gibbs to join forces with him and try the ‘‘brainwave’’ equipment as a potential means of studying epilepsy [8]. Frederic Gibbs (1903–1992) had come from Johns Hopkins University to work with William G. Lennox (1884–1960), already a well-known epileptologist, at Boston City Hospital. Lennox and Gibbs had been frustrated in their work on a circulatory hypothesis of seizures. They demonstrated no cerebral anoxia with seizures; however, their techniques remain pioneer work in cerebral blood flow studies [3]. Erna L. Gibbs, an immigrant from Germany, was originally a technical coworker of Lennox, married Frederic Gibbs, and was one of the world s first EEG technicians and co-author of many papers and texts. Epilepsy & Behavior 3 (2002) 393–394

Peter Emanuel Dans, MD: A Conversation with the Editor

Peter Dans (Figure ​(Figure11) was born in New York City on June 17,1937. After attending Catholic elementary schools, high school, and college, he graduated from Columbia University College of Physicians and Surgeons in 1961. His internship and first-year residency were on the Osier Medical Service of The Johns Hopkins Hospital, during which he spent 3 months at an infectious disease hospital in Calcutta, India. A medical residency year at the Presbyterian Hospital of the City of New York was followed by 3 years in the US Public Health Service as a research associate in the Laboratory of Viral Diseases of the National Institutes of Health (NIH) and a 2-year fellowship at the Thorndike Memorial Laboratory of the Boston City Hospital in infectious diseases.

A career in cerebrovascular disease: a personal account.

The Editor, when inviting this piece, thought that an account of my entry into the stroke field and the unfolding of the subsequent studies in cerebrovascular disease would be instructive for the younger readers of Stroke . Be that as it may, knowledge of how a specialty has evolved can be useful in placing present endeavor in perspective. The story is one of clinical and neuropathological studies carried out by one person, an approach now largely superseded. In 1949, after my completing a fellowship in Neurology at the Montreal Neurological Institute, Dr Wilder Penfield recommended a year of postgraduate work abroad. Dr Roy Swank, a colleague, insisted that a period of study on the Neurology Service of the Boston City Hospital (BCH) under the direction of Dr Derek Denny-Brown and Dr Raymond D Adams would be unparalleled. Dr Swank placed a telephone call and in a minute or two it was arranged that I spend a year in Neuropathology at BCH under the guidance of Dr Adams. The subject to be investigated was acute hypertensive encephalopathy. A grant-in-aid was received from the Multiple Sclerosis Society. It was for $100. In 1949 BCH was one of the world’s premier medical centers: 2000 beds and 3 academic medical services, Harvard Medical School, Boston University, and Tufts Medical School. Enthusiasm was the order of the day. The Department of Pathology, including the Section of Neuropathology, comprised the Mallory Institute of Pathology. It was a busy service, with 900 autopsies performed each year. In addition, the Coroner’s Office was housed in the Institute. In Neuropathology 700 to 800 brains were examined yearly. The abundance of pathological material would be an important factor. Two residents in Neuropathology were responsible for the day-to-day work: Dr David McDougall, the senior, and myself. Dr McDougall developed formalin dermatitis …

Why Heal-In Worked

Back to table of contents Previous article Next article Letter to the EditorFull AccessWhy Heal-In WorkedLawrence B. Mutty, M.D., M.P.H.Lawrence B. MuttySearch for more papers by this author, M.D., M.P.H.Published Online:19 Oct 2001https://doi.org/10.1176/pn.36.20.0024aI read with interest Dr. Avram Mack’s article in the July 20 issue titled “Treading Carefully on the Path to Union Membership.” My wish is only to offer a different perspective on the 1967 “Heal-In” at Boston City Hospital. I was at the time a chief resident in psychiatry on what was then a Harvard service. I recall no mention of proposed union affiliation or concern about compensation, since the vast majority of residents felt privileged to be training under such notable clinicians as Dr. Derek Denny-Brown.At issue were deplorable conditions for patient care such as grimy, open-bay wards with water-filled grapefruit juice cans filled with cigarette butts, an absence of bed linen, and no assistants to transport patients for X-ray studies or other procedures, such that interns had to push the gurney stretchers themselves.The city administration had turned a deaf ear to the repeated pleas of the interns and residents. The “heal-in” was a last-ditch effort to draw public attention to the plight of the patients, who were, many of whom were poor and African Americans. We were determined during the heal-in to provide superior round-the-clock care. I recall being on duty for 36 hours straight. There were no “nonpatients” admitted, as described in Dr. Avram’s article. Rather, the decision was made not to discharge patients until every outstanding laboratory or X-ray study result was on the chart—this was had also been a significant problem in the precomputer era because of an absence of lab result dispatchers.The Boston Globe was contacted in advance, emphasizing that superior care would be provided to patients during the heal-in. Thus, there was widespread public sympathy and support for this effort.As I recall, the patient census soared from 800 to the full 1,200-bed capacity in two days. This required that some patients seeking admission were temporarily deferred to Massachusetts Memorial and Massachusetts General, New England Medical Center, and other area hospitals.The city of Boston finally got the message, and the necessary patient care improvements were initiated.This was not an action taken lightly and indeed only as a last resort. The interns and residents at Boston City Hospital felt totally vindicated by these positive results.Castine, Maine ISSUES NewArchived

Carleton B. Chapman, MD, MPH

Carleton B. Chapman, who made important contributions in 4 areas of medicine, died in Hanover, New Hampshire, on December 10, 2000. These areas included cardiovascular medicine and research, medical education, philanthropy, and medical history and ethics. His career can be separated temporally into periods when he focused on each of these areas, although he was active in all of them throughout his career. Dr Chapman was born on June 11, 1915, in Sycamore, Alabama (the same small community that produced Tinsley Harrison). He attended public schools in Talladega and graduated from Talladega High School. He was a precociously talented concert organist during his school years, and he seriously considered a career in music. Although he ultimately chose medicine, he maintained his passion for playing the organ throughout his life. He entered Davidson College in 1932 as a liberal arts major, where he became President of the Student Body and a member of Phi Beta Kappa. By the time of his graduation in 1936, he had developed an interest in human physiology, which he pursued at Oxford University after being awarded a Rhodes Scholarship. As a student of St Johns College, Oxford, from 1936 to 1939, he received his BA and MA degrees in Physiology. During that time, he worked with the famous respiratory and exercise physiologist Professor C.G. Douglas. He returned to the United States in 1939 and completed medical school at Harvard, where he received his MD in 1941 and his MPH in 1944. His training in Internal Medicine and Cardiology was received at Boston City Hospital from 1941 to 1944. From 1944 to 1946, he was in the Public Health Service and was stationed first in the Middle East and then in China and Indonesia. In 1946, he returned to Harvard and did a second …

Ramzi S. Cotran, MD

HomeCirculationVol. 103, No. 4Ramzi S. Cotran, MD Free AccessObituaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessObituaryPDF/EPUBRamzi S. Cotran, MD L. Maximilian Buja L. Maximilian BujaL. Maximilian Buja Search for more papers by this author Originally published30 Jan 2001https://doi.org/10.1161/01.CIR.103.4.482Circulation. 2001;103:482Dr Ramzi S. Cotran (1932–2000), who is widely acknowledged as one of the foremost and most distinguished academic pathologists in the United States, died October 23, 2000, at his home in Brookline, Massachusetts at the age of 67.His pioneering work with endothelial cells and vascular smooth muscle cells in tissue culture, performed with Drs Michael Gimbrone and R. Judah Folkman, made him one of the founders of the modern field of vascular biology. He exerted an enormous impact on both vascular biology and nephrology research while building the Department of Pathology at Brigham and Women’s Hospital into an international leader in academic pathology during his 27 years at its helm.The fact that more than 500 people came to Brigham and Women’s Hospital from as far away as Amsterdam to salute Dr Cotran last September when the Cotran Professorship in Pathology at Harvard Medical School was announced speaks volumes to the respect and admiration he earned over a lifetime.At the time of his death, Dr Cotran was chairman of the pathology departments at Brigham and Women’s Hospital and Children’s Hospital in Boston and was the Frank B. Mallory Professor of Pathology at Harvard Medical School. He was named pathologist-in-chief at Peter Bent Brigham Hospital in 1974 and, during nearly 3 decades, he transformed his department from a small clinical service into a distinguished academic department that is widely considered one of the nation’s best training programs for pathology.Born in Haifa, Palestine, Dr Cotran received his medical degree from the American University of Beirut in 1956. He came to the United States for postgraduate training in pathology and nephrology at Boston City Hospital’s Mallory Institute of Pathology in Boston and at Memorial Sloan-Kettering Cancer Center in New York.Many will remember him through his publications. In 1979, he became the senior author of Robbins Pathologic Basis of Disease, one of the most widely read textbooks in medicine.His contributions to the medical and scientific discipline of pathology were immense. He served as president of the American Association of Pathologists, president of the United States and Canadian Academy of Pathology, a trustee of the American Board of Pathology, and a member of the Residency Review Committee for Pathology.One of Dr Cotran’s most important contributions to medicine was his teaching. He mentored and trained many of the most talented pathologists today. More than a dozen departmental chairs trained with him and learned both their technical and leadership skills from his teaching and example. His forward thinking made him one of the giants in the field and influenced all who were fortunate enough to know him. Harvard also recently gave him a Lifetime Achievement Award in Mentoring and the Dean’s Award for Support and Advancement of Women Faculty in recognition of his many contributions.He also recently received the John P. Peters Award from the American Society of Nephrology for his research into the mechanisms of immune, infectious, and vascular renal injury; his training program; and his long-standing leadership role in academic renal pathology. The author of more than 180 research papers, he was an elected member of the Institute of Medicine of the National Academy of Sciences and the American Academy of Arts and Sciences.Dr Cotran is survived by his wife, Kerstin; son, Paul Cotran, MD; daughter Leila Cotran Jacobs and her spouse Marc; daughter Nina Cotran, MD, and her spouse David Lenrow; daughter Suzanne Williamson and her spouse Donald; and 11 grandchildren.Simply stated, Dr Cotran was a pathologist’s pathologist, a superb mentor, and a teacher for all of medicine, and he will be greatly missed.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetails January 30, 2001Vol 103, Issue 4Article InformationMetrics Copyright © 2001 by American Heart Associationhttps://doi.org/10.1161/01.CIR.103.4.482 Originally publishedJanuary 30, 2001 PDF download Advertisement

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