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Notable Contributions[edit]

The discovery of insulin[edit]

The discovery of insulin in 1921 by two young investigators at the University of Toronto, Professors Frederick Banting and Charles Best, was one of the most important medical achievements of the twentieth century. [1] Prior to the discovery of insulin there was no way to treat diabetics. Today, the lives of millions worldwide are saved through the use of this hormone.[2]

The discovery of the baby food Pablum[edit]

In 1930, Professors Frederick Tisdall, Theodore Drake and Alan Brown invented Pablum, a processed cereal containing essential nutrients for infants. It revolutionized infant nutrition and helped prevent rickets.[3] In 1929, Tisdall and Drake began to intensify and expand their experiments with animals, and tested foods on groups of children in the hospital and in orphanages. At that time infants were being fed cereal and biscuits consisting mostly of wheat, oats or corn meal. All the bran and germ had to be removed because whole grain cereal was difficult for a baby to digest. The doctors discovered how to make a mixture that would contain all the essential vitamins and minerals that babies needed, yet wouldn't cause undue constipation or diarrhea. They added ingredients such as honey to make it more palatable and baked it into a biscuit, but soon realized that tiny babies couldn't eat biscuits. A cereal was needed that could be mixed with milk and spoon-fed, so they produced a cereal that had many of the same ingredients as the biscuits. For three months babies and older children in the hospital were fed on the mixture. They liked it, they didn't become constipated and their health improved, but the cereal had one serious drawback: it required lengthy cooking. About this time the practice of drying milk by letting it drip on a red-hot revolving drum and immediately scraping it off was coming into use, so the researchers tried this technique with their cooked cereal and it worked. The mixture came off the drum as a bone-dry, flaky powder. Now they had a baby food that filled all their requirements and would keep indefinitely. They called it Pablum.[4]

The production and evaluation of diphtheria toxoid[edit]

Until the mid-1920s diphtheria, often called "the strangler," was the scourge of childhood, ranking first as a cause of death for children under 14. Despite the introduction and free distribution in Canada of Connaught's diphtheria antitoxin after 1914, incidence remained stubbornly high. The key to its defeat was diphtheria toxoid, discovered by Dr.Gaston Ramon of the Pasteur Institute in 1924. Connaught Laboratories were the first to produce the new toxoid on a large scale and scientifically test its effectiveness during a series of Canadian field trials between 1926 and 1931. In the wake of these trials diphtheria incidence declined sharply in such cites as Toronto and Hamilton, dropping effectively to zero cases and zero deaths by the early 1930s. This pioneering Canadian public health effort represented the first statistical demonstration of the value of a non-living vaccine in preventing a specific disease. [5] Central to this effort was Connaught's founder, Professor John G. FitzGerald, who was determined to stamp out diphtheria. Indeed, Connaught was born out of his obsession with providing diphtheria antitoxin at a cost that was "within reach of everyone." In 1924, a few months after Dr.Ramon's discovery, during one of his many visits to the Pasteur Institute in Paris, FitzGerald became so impressed by the new toxoid that he immediately called Professor Peter J Moloney at Connaught. FitzGerald described Ramon's methods to Moloney and asked him to drop everything and immediately begin preparing the toxoid. Despite a few early problems, Moloney was quickly able to produce a safe, potent and plentiful supply that was ready to be tested in children. In 1925, Moloney also made a major contribution to the wide acceptance of the toxoid by developing a "reaction test" to identify those who would likely react to a full dose of toxoid. Such reactors would then receive a diluted toxoid shot, but with the same immunizing effect.[6]

The development of heparin[edit]

The University of Toronto, Faculty of Medicine was central to the development of heparin, providing the first reliable and inexpensive means to control blood clotting, making possible a wide range of life-saving surgical interventions. Heparin is a powerful blood anticoagulant that is essential for open heart surgery, organ transplants and for treating dangerous internal blood clots, or thrombosis, which can block blood flow to the lungs with sudden and fatal results.[7].Heparin was discovered in 1916 at Johns Hopkins University, but it was not practically applied by doctors until the early 1930s when a research team at Connaught Laboratories developed a method to make available a purified, plentiful and inexpensive supply safe for human use. The heparin project began in 1928-29 and was spearheaded by Professor Charles H. Best. At the time only small amounts of heparin, made from dog liver, was available, but it was extremely expensive, toxic and unsafe for humans. The first phase of the heparin project involved the production and standardization of a purified product by Professors Arthur F. Charles and David A. Scott. In 1935, Professor Gordon Murray began the first human surgical trials of heparin. Charles and Scott's first task was to find a cheaper source of heparin than dog liver. They turned to beef liver, readily available from local slaughterhouses, and were successful in extracting significant amounts of heparin. However, a growing pet food industry drove up the price of beef liver, forcing them to try other tissues. They found that beef lung and intestines were also good sources of heparin; the latter more plentiful and cheap as it was less useful for pet foods. Between 1933 and 1936, they succeeded in purifying and then crystallizing heparin into a standardized dry form that could be administered in a salt solution.[8] Heparin thus became Connaught's second product, after insulin, to be recognized as an international biological standard. By 1937 it was clear that Connaught's heparin was a safe, easily available and effective blood anticoagulant.

The discovery of the first mobile blood transfusion Unit[edit]

In the 1930s, Professor (Henry) Norman Bethune spearheaded the implementation of the first practical mobile blood collection and distribution system. His approaches were novel and entirely without precedent, and shaped blood transfusion practices throughout the world.[9] In 1936, Bethune was invited to lead a surgical team in Spain to care for casualties in the Spanish Civil War. There he was influenced by the Barcelona Blood Transfusion Service which was sending citrated blood to the front. However, there was no systematic provision of blood, and too many men were dying of blood loss in military hospitals. Bethune recognized the need for a centralized service for collecting blood and for delivering it to the front for immediate transfusion. He devised a specialized vehicle with a kerosone-run refrigerator, a sterilizing unit, and other equipment required for on-site transfusion, thus creating the Canadian Blood Transfusion Service. The first deliveries started on December 23, 1937. Within 5 months, the organization was supplying a 1000 km long war front with up to 100 transfusions per day, using a staff of over 100, about 4000 blood donors and 5 custom-built blood delivery trucks.[10] During the course of the war that ended in 1939, this organization – the precursor of Mobile Army Surgical Hospital (MASH) units that were used in the Korean War – transfused approximately 5000 units of blood.

Contribution to the Salk polio vaccine[edit]

In 1945, Professor Raymond Parker discovered a defined chemical nutrient medium in which cells could grow and replicate. This discovery and work by other polio researchers at the Connaught Medical Research Laboratories later contribute to Jonas Salk's development of the Salk polio vaccine.[11] During the early 1950s, the University of Toronto played a significant role in bringing the growing scourge of Polio under control, contributing several essential elements to producing a safe and plentiful supply of the Salk inactivated polio vaccine. “Medium 199” – the world’s first synthetic tissue culture medium – proved ideal for cultivating the poliovirus for a human vaccine. And “The Toronto Method” developed by Professor Leone N. Farrell for large-scale production of the poliovirus, made it possible to test the Salk polio vaccine through the largest field trial in medical history in 1954.[12]

Discovery of the first electronical heart pacemaker[edit]

Since its invention in 1951, the heart pacemaker has improved the lives of millions of people, including the Canadian engineer who invented it.[13] The invention of the pacemaker was unintentional -- it came out of research into “cold heart surgery” in the 1940s by Canadian surgeons, Professors Wilfred G. Bigelow and John Callaghan at the Banting Institute in Toronto.[14] Bigelow believed that the only way cardiovascular medicine could advance was by enabling open-heart surgery. Based on his experience as a field medic during World War II, he was convinced that cooling the body and slowing the heart rate was the way to go. One of the challenges the two surgeons faced was keeping the heart beating while the body was hypothermic. During an experimental surgery on a dog, they noticed that stimulating a stopped heart with an electrical probe could restart it, and that sending pulses of electrical current could actually change the heart’s rate. To turn this discovery into a clinical device, Bigelow and Callaghan recruited John Hopps, an electrical engineer from the National Research Council of Canada. The first pacemaker, built by Hopps in 1949, was a bulky device that used vacuum tubes to generate electrical pulses. An insulated wire inserted through the jugular vein delivered the electric shocks to the right atrium of the heart. These shocks provided the artificial pacing.Today’s pacemakers are about the size of a USB stick. Pacemaker surgery is usually performed in less than an hour under a local anesthetic and most people return to normal activities within a few days.[15]

Advancements in diagnosing and treating Hodgkin's disease and breast cancer[edit]

The treatment of Hodgkin’s disease and breast cancer were significantly advanced in Toronto through the radio therapeutic research and treatment methods pioneered by Professor M. Vera Peters.[16] By the early 1950s, Peters’ research clearly demonstrated the importance of early diagnosis and radiation treatment against Hodgkin’s disease. Her landmark publication in 1950 showed that a high proportion of patients with early-stage Hodgkin’s disease – considered incurable at the time – could be cured if treated with high dose radiation. From 1958 to her retirement in 1976, Peters worked at the Princess Margaret Hospital where her relentless pursuit of scientific truth with respect to treating early-stage cancer of the breast proved that breast-conserving surgery (lumpectomy) followed by radiation is as effective as radical mastectomy.[17] Her findings in both Hodgkin’s disease and breast cancer, although initially met with skepticism, became common practice throughout Canada and the world.

The discovery of the stem cell[edit]

The stem cell story began in 1958 with the building of the University of Toronto's Department of Medical Biophysics, attracting hematologist Professor Ernest McCulloch and biophysicist Professor James E. Till, who are known as the “fathers of stem cell research” because they proved the existence of stem cells and characterized them.[18] This significantly altered the landscape of cell biology, especially cancer research. Their efforts focused on the biological effects of radiation on cancer cells by replacing dead bone marrow cells with healthy cells. They observed the transplanted cells developed “colony forming units” that proved to be self-renewing precursors of new blood cells, later called a “stem cell.” [19] This dynamic team revolutionized medical literature, uncovered new ways to treat many diseases, and laid the foundation for bone marrow transplantation. In 1961, they published a paper which proved the existence of stem cells. In 1963, they defined the two key properties of stem cells: stem cells have the capacity for self-renewal, and stem cells can differentiate into more specialized cells.

The development of continuous passive motion (CPM) treatment[edit]

After completing his residency, Professor Robert Salter moved to Britain for fellowship training, where he was taught that immobilization for fractures should be complete, rigid, enforced and prolonged. During the past 22 centuries, the traditionally accepted and enforced treatment for diseased and injured joints was immobilization. Yet the potential for joint cartilage to heal or to regenerate is notoriously limited.[20] Salter’s intuition told him that this dogma was false, and he challenged this concept, applying basic science principles to identify deleterious effects of joint immobilization. In 1960 he developed an operation for hip dislocation in children, known as the "Salter Operation".[21] In 1970, he concluded from his previous 15 years of research that immobilization was very harmful to joints and furthermore, that immobilization did not stimulate joint cartilage either to heal or to regenerate. Consequently he originated the revolutionary biological concept of continuous passive motion (CPM) of joints. In 35 experimental investigations, he demonstrated that CPM for four weeks has a remarkably beneficial effect on the healing and regeneration of joint cartilage. Since 1978, Salter began to apply CPM to the care of human patients while continuing his research. John Saringer, a mechanical engineer and researcher from U of T began working with Salter to produce CPM machines for all the synovial joints of the body. Salter continued his philosophy that fundamental science provides the basis for the development of new therapies in his work understanding the pathophysiology of hip dysplasia, resulting in his development of the Salter Innominate Osteotomy, a procedure that is now used worldwide. His observation of pediatric fracture patterns and their risk of growth arrest played a role in the development of the Salter-Harris classification of growth plate injuries.[22]

The discovery of Glycemic Index of foods[edit]

The Glycemic Index (GI) is a scale that ranks carbohydrate-rich foods by how much they raise blood glucose levels compared to a standard food. Before 1981, all patients diagnosed with diabetes were given dietary exchanges to follow when planning their meals or snacks. While exchanges were formulated for all food groups, the main focus for glycemic control was on carbohydrates. Professor David Jenkins challenged the assumption promoted by the exchange system that all simple carbohydrates caused a rapid rise in blood glucose levels and all complex carbohydrates released glucose more slowly into the blood. He set out to investigate exactly what happens when the body digests carbohydrates.[23] He did this in the most logical way he could think of—by actually giving a predetermined amount of some commonly consumed carbohydrate foods to his subjects to eat and recording their resulting blood glucose levels after a designated period of time. Jenkins and his colleagues discovered that in equivalent quantities, carbohydrates in white bread (a complex carbohydrate) elevated their subjects’ blood glucose more than those in ice cream, despite its sugar (a simple carbohydrate) content. This seemed to fly in the face of the exchange system and the conventional wisdom of the time.As other scientists began testing more carbohydrate foods using the same methods, the results were tabulated and slowly were compiled into what we today call the Glycemic Index (GI). A review of the nearly 700 foods currently listed in the Glycemic Index underscores the limitations of the exchange concept; the amount of carbohydrate in two similar foods may be the same, but their impact on blood glucose levels can be very different.

Pioneering the use of aspirin[edit]

Professor Henry Barnett recognized that assumptions about the treatment of stroke were made, that these assumptions should be questioned, and that the answers, so important to millions of people, must be obtained in very large clinical trials of absolute integrity.[24] He first addressed the preventive use of aspirin, alone and in comparison with other platelet-inhibiting agents. Barnett pioneered the use of aspirin as a preventive therapy for heart attack and stroke.[25]

The first single and double lung transplant[edit]

In 1963, Professor F. Griffith (Griff) Pearson began a series of lung transplantation experiments at the University of Toronto. With a surgical team that included Professor Joel Cooper, an initial attempt to transplant a lung was made in 1977, although it was unsuccessful. By November 1983, after Professor G. Alexander Patterson joined the Toronto transplant group, the world’s first successful single lung transplant was performed, followed by the first double lung transplant in 1986.[26]

Development of valve-sparing aortic root replacement[edit]

The aortic root is the section of the aorta (the large artery leaving the heart) that is attached to the heart. The aortic root includes the annulus (tough, fibrous ring) and leaflets of the aortic valve; and the openings where the coronary arteries attach. An aneurysm is an abnormal bulge in the wall of a blood vessel. In some patients, an aneurysm can occur at the aortic root, causing the aorta to dilate or widen and the aortic valve to leak. Without treatment, a life-threatening condition called aneurysm dissection can occur. In this condition, blood flows through a tear in the inner layer of the aorta, causing the layers to separate. Blood flow becomes interrupted and causes the arterial wall to burst. Professor Tirone E. David developed numerous operative procedures to treat patients with heart valve disease, complications of myocardial infarction, and thoracic aneurysms. He pioneered the valve-sparing aortic root replacement, a method of surgical treatment for aortic root aneurysms.[27] With this method, the aneurysm is repaired while the patient's own aortic valve is preserved. This method helps to avoid the use of long-term anticoagulant (blood-thinner) medication and may reduce the risk of stroke. If the patient's own aortic valve is diseased or cannot be used during the aorta surgery, a bioprosthetic valve can be used to avoid the use of long-term anticoagulation.

The discovery of the T-cell receptor gene[edit]

Professor Tak Wah Mak became a world-renowned researcher in 1984, when he identified the gene that is responsible for making T-cell receptors in the body. T-cells are the body’s defense cells, which help fight viral infections, “Helper” T-cells possess receptors that can identify viruses, and signal “killer” T-cells to attack.[28] In discovering the gene that controls the production of these receptors, Mak made an enormous breakthrough in the understanding of the body’s immune system. The T-cell receptors are possibly the most important element of the immune system –they allow T-cells to distinguish “self” from “non-self.” Identifying this gene may lead to better treatments for a whole host of immune-disorders and other related conditions, from diabetes to cancer.

First sciatic nerve transplant[edit]

The sciatic nerve contains many thousands of axons, some that convey messages from the spinal cord to the muscles and other axons convey messages in the opposite direction, taking information from the skin to the spinal cord. Thus, if the nerve is irreparably damaged, the muscles supplied by that nerve will not be able to work, and the area of the skin supplied by that nerve will be anaesthetic. In 1970, Professor Alan Hudson studied the way in which nerves regrew through autografts and Professor Susan MacKinnon established testing methods so that the degree of rejection of the transplanted nerve graft could be measured. MacKinnon then conducted a series of experiments in which the rejection phenomenon was suppressed, so as to allow regrowth through the nerve grafts in a manner analogous to regrowth through autografts. On 25 September 1988, a 16-year-old female died from a hemorrhage into the brain in London, Ontario. Her family gave permission to harvest the organs, and the nerves were then rushed to Toronto, where they were sewn in under the operating microscope from the buttock to the knee to replace the damaged nerve in a patient. The patient received immunosuppressive drugs according to the regimes that had been established in the years of experimental work with animals.[29] Two years after the surgery, the patient was able to feel a pinprick on the sole of his foot for the first time since the boating accident that had destroyed his sciatic nerve, thus proving that the axons had successfully grown through the graft and down the nerves to the sole of the foot. The immunosuppressive drugs were then stopped and, to everyone's great relief, the clinical improvement already noted did not change.

The discovery of the Cystic Fibrosis gene[edit]

Professor Lap-Chee Tsui’s discovery of the Cystic Fibrosis gene improved our understanding of how the disease works, led to newborn screening for early detection of CF and carrier testing for parents.[30] It also opened the door to research targeting the root cause of the disease in hopes of finding more effective treatments and, one day, a cure.Tsui became internationally acclaimed in 1989 when he and his team identified the defective gene, namely Cystic fibrosis transmembrane conductance regulator (CFTR), that causes cystic fibrosis, which is a major breakthrough in human genetics. [31] He has also made significant contributions to the study of the human genome, especially the characterization of chromosome 7, and, identification of additional disease genes.[32]

The cell receptor discoveries leading to the development of new cancer drugs[edit]

A 1991 team led by Professor Anthony Pawson identified how cell receptors transmit signals instructing the cell to change. Pawson's discoveries contribute to every aspect of medical research and have relevance for the understanding and treatment of a host of diseases including cancer, diabetes, and disorders of the immune system.[33] His insights on cancer cell signaling (namely, how to “switch off” growing cancer cells) have underpinned effective new approaches to cancer treatment.In particular, Pawson studies signal transduction – the way in which cells control their own and each other’s behavior through chemical signals.[34] Many disease processes such as diabetes, heart disease, autoimmunity and cancer arise from defects in signaling. Pawson’s groundbreaking discoveries related to signal transduction allowed for the development of a new generation of drugs that halt the proliferation of some kinds of cancer cells.

Discovery of two genes responsible for early-onset Alzheimer’s[edit]

In 1992, Professors Peter St George-Hyslop and Don Crapper McLachlan reported that a previously unidentified gene in chromosome 14 causes early-onset of Alzheimer’s disease.[35] In 1995, St George-Hyslop led the team which identified this gene on chromosome 14 (presenilin 1). A few months later he also discovered a second similar gene (Presenilin 2 - located on chromosome 1), which was responsible for a less severe form of familial early-onset Alzheimer's disease. In 2000, St George-Hyslop, and his team of researches identified a key protein that causes nerve cell degeneration. Although more studies and tests are required, these findings could lead to a new drug that would regulate the progression of Alzheimer disease.[36] Until recently, only four genes associated with late-onset Alzheimer's were confirmed, including SORL1, which was discovered at the Tanz Centre at U of T in 2007 by a team of researchers again lead by St George-Hyslop.[37] In 2011, a consortium of Alzheimer's researchers, including a team from Canada, which included St George-Hyslop, identified five additional genes that each add to risk of dementia later in life.[38]

The discovery of new therapy for Retino-Blastome[edit]

In 1996 Professor Brenda Gallie and her team developed a new therapy for retinoblastoma, a cancer of the eye that leads to blindness, which represents the first major change in management of the disease in 35 years.[39]Gallie's discoveries have not only improved the outcomes of children and families with retinoblastoma worldwide, they have also revealed fundamental mechanisms underpinning the basic molecular genetics of cancers in general. In the 1980s, Gallie and her collaborators discovered that retinoblastoma arises in the retina of children when a gene called RB1 becomes mutated and stops its normal function of suppressing cancer. When others later cloned the RB1 gene, Gallie set out to develop highly sensitive ways to find the exact mistake in RB1 causing cancer in each clinical case.

Pioneering the XVIVO lung perfusion system[edit]

The Toronto XVIVO Lung Perfusion System is a world-first technique developed by a team of researchers led by Professor Shaf Keshavjee. It was first applied clinically in 2008 and gives surgeons the opportunity to make injured donor lungs suitable for transplantation.[40]

Identification of the cancer stem cell[edit]

Cancer stem cells were first identified in certain types of leukemia in 1997 by Professor John Dick and colleagues at the University of Toronto. The cells were harder to spot in solid tumors because biologists did not possess the means of recognizing the markers — characteristic proteins on the surface of a cell — that had been developed for a stem cell that makes red and white blood cells.[41] Dick and his team investigated the genetic programs that control human blood stem cells (HSCs) to determine how changes in these programs lead to generating leukemia initiating cells. Dick’s lab developed a novel NOD/SCID xenotransplant assays for human HSCs and primitive progenitors and methods for modeling initiation and progression of leukemia through genetic manipulation that have provided insight leukemia development. Most recently, scientists have showed that the genetic characteristics of leukaemia-initiating cells from acute myeloid leukemia (AML) patients are better at predicting clinical outcome than the majority of AML cells. This is the first time it has been described that leukemia initiating cells are significant not just in experimental models but also for patients. Dick's team has also discovered that genetic diversity occurs in functionally defined leukaemia-initiating cells and that many diagnostic patient samples contain multiple genetically distinct leukaemia-initiating cell subclones. This will likely be extremely important when considering personalized medicine strategies. His team has also isolated a human blood stem cell in its purest form – as a single stem cell capable of regenerating the entire blood system.[42] This breakthrough opens the door to harnessing the power of these life-producing cells to treat cancer and other debilitating diseases more effectively.

Understanding cell division[edit]

Professor Yoshio Masui, whose experimental work has focused on frogs, discovered a protein, called maturation promoting factor (MPF), in the cytoplasm of cells that control cell division in the fertilized eggs of frogs. As a young man, Yoshio Masui took a sabbatical from Konan University in Japan to study enzymes that control development in a laboratory at Yale, where his work on frog oocytes began. Initial studies showed that division of a cell that will give rise to an egg (an oocyte) could be stimulated by the hormone progesterone, but it only worked when the surface of the eggs were exposed to progesterone—not when the hormone was injected directly into the oocytes. He concluded that progesterone acting on the egg's surface must affect something in the cytoplasm of the cell that, in turn, stimulates cell division. He set out to find that "something," which turned out to be an activity in the cytoplasm that he called MPF, without knowing precisely what it was. After his sabbatical at Yale, Masui continued his research at the University of Toronto and found that MPF is a protein.[43] Masui developed techniques for preparing highly concentrated extracts of egg cytoplasm, which then made it possible to analyze cell cycle processes biochemically, and to purify MPF.

The invention of Supplefer Sprinkles[edit]

In 2002, Professor Stanley Zlotkin invented Supplefer Sprinkles, a tasteless, inexpensive powder that can be added to any food and that helps eliminate childhood anemia in developing countries.[44] Supplefer Sprinkles are single-serve sachets of tasteless dry powder that consists of vitamin C and encapsulated iron. Other micronutrients (such as the B vitamins, vitamins A, D and E; folic Acid, zinc, copper and iodine) may also be added.[45] Supplefer Sprinkles are intended to be "sprinkled" or stirred into any food-including rice, barley, congee or porridge. Each sachet is a single dose and does not require special measuring or handling.

Restoration of sight to blind mice with stem cells[edit]

Only recently did scientists discover that the retina of an adult also contains versatile stem cells. For years experts believed that unlike fish and frogs, mammals had no capacity to rally replacement cells in the retina once they were damaged. But in 2000, Professor Derek van der Kooy's group published a landmark paper proving stem cells exist in the retinas of adult mice, just as stem cells were surprisingly discovered to exist in the adult brain.[46]Van der Kooy and colleagues identified stem cells in a part of the retina closer to the front of the eye. In 2010, his team published a paper describing how they restored sight to the eyes of three blind mice by using stem cells salvaged from the retinas of human cadavers.[47] The feat has been repeated several times over and marks an important step toward the goal of restoring sight in people.

The world's largest health study[edit]

Professor Prabhat Jha leads the world's largest health study of millions of people. He is working with the Governments of India, Canada and the USA on the largest ever study of smoking and death in India. He is the principal investigator of a prospective study of 1 million deaths in India, researching mortality from smoking, alcohol use, fertility patterns, indoor air pollution, and other risk factors among 2.3 million homes and 15 million people.[48] Jha spearheaded an 11-year-old initiative known as the Million Death Study – an effort to figure out how one million Indians, mostly poor, mostly rural, died – and to use that information to evaluate and possibly redirect health policy. Its findings have proved so valuable that it is now expanding across the developing world. Understanding the cause of death is important for public policy: given the absence of data, much of health policy in India and other countries has been, up until now, formulated based on estimates from United Nations agencies or research by donors about what kills people. The “Million Death Study” is the first nationally representative study of the effect of tobacco-smoking on health that covered more than one million households. Prior to the study, it was assumed that smoking risks were widely known because of the studies from Europe and the USA.[49] In the study, causes of death have so far been identified for 350,000 people – and challenged the conventional wisdom on how Indians die, showing a far greater role for smoking, snake bites and suicide, and a far less significant one than was assumed for AIDS.[50]

Pioneering in the role of MRI and focal therapy in the treatment of prostate cancer[edit]

Dr. Larry Goldenberg, who completed his medical training at the University of Toronto in 1978, is a pioneer of the role of MRI and focal therapy (treatments that target individual spots of prostate cancer instead of the entire gland). He pioneered the use of intermittent hormone withdrawal, which is now considered a standard treatment option for prostate cancer. He also developed a low dose antiandrogen/DES protocol that was the principal therapy used in British Columbia for advanced prostate cancer until the mid-90′s.[51] His work has led to numerous clinical trials, with the promise of bringing innovative treatment alternatives to men with prostate cancer. He’s now focusing on patient education and decision making, the evaluation of MRI in prostate cancer diagnostics, the development of multiparametric ultrasound, the role of active surveillance in early stage cancer, the potential use of focal therapy, advances in robotic surgery and a variety of new treatments for benign prostatic hyperplasia.[52]

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