University Professor and Director
Johns Hopkins Malaria Research Institute
Baltimore, Md.

A native of Minnesota, Peter Agre studied chemistry at Augsburg College  (B.A., 1970) and medicine at Johns Hopkins (M.D., 1974). He completed his residency at Case Western Reserve University in Cleveland and an oncology fellowship at the University of North Carolina at Chapel Hill.

Agre joined the Johns Hopkins School of Medicine faculty in 1984 and rose to the rank of professor of biological chemistry and professor of medicine. In 2005, Agre moved to the Duke University School of Medicine where he served as vice chancellor for science and technology and James B. Duke Professor of Cell Biology. Agre returned to Johns Hopkins in January 2008, where he is professor and director of the Malaria Research Institute at the Bloomberg School of Public Health.

In 2003, Agre shared the Nobel Prize in Chemistry for discovering aquaporins, a family of water channel proteins found throughout nature and is responsible for numerous physiological processes in humans and is implicated in multiple clinical disorders. Agre has received other honors including 12 honorary doctorates, Commandership in the Royal Norwegian Order of Merit from King Harald V, and the Distinguished Eagle Scout Award from the Boy Scouts of America. Agre is a member of the National Academy of Sciences and the Institute of Medicine, for which he chaired and serves on the Committee on Human Rights. In February 2008, Agre became president-elect of the American Association for the Advancement of Sciences.

University Professor and Director
Johns Hopkins Malaria Research Institute
Baltimore, Md.

A native of Minnesota, Peter Agre studied chemistry at Augsburg College  (B.A., 1970) and medicine at Johns Hopkins (M.D., 1974). He completed his residency at Case Western Reserve University in Cleveland and an oncology fellowship at the University of North Carolina at Chapel Hill.

Agre joined the Johns Hopkins School of Medicine faculty in 1984 and rose to the rank of professor of biological chemistry and professor of medicine. In 2005, Agre moved to the Duke University School of Medicine where he served as vice chancellor for science and technology and James B. Duke Professor of Cell Biology. Agre returned to Johns Hopkins in January 2008, where he is professor and director of the Malaria Research Institute at the Bloomberg School of Public Health.

In 2003, Agre shared the Nobel Prize in Chemistry for discovering aquaporins, a family of water channel proteins found throughout nature and is responsible for numerous physiological processes in humans and is implicated in multiple clinical disorders. Agre has received other honors including 12 honorary doctorates, Commandership in the Royal Norwegian Order of Merit from King Harald V, and the Distinguished Eagle Scout Award from the Boy Scouts of America. Agre is a member of the National Academy of Sciences and the Institute of Medicine, for which he chaired and serves on the Committee on Human Rights. In February 2008, Agre became president-elect of the American Association for the Advancement of Sciences.

Clinical Professor, Section of Pediatric Cardiology
Principal Investigator, Bogalusa Heart Study
Tulane University School of Medicine/School of Public Health
New Orleans, La.

Investigations led by Dr. Berenson in Bogalusa for 30 years, involving thousands of children in rural Louisiana, have provided what amounts to an encyclopedia of the critical early natural history of arteriosclerosis and hypertension. His findings have provided solid evidence of the need to look for emerging sings of cardiovascular and metabolic abnormalities and to aggressively address modifiable risk factors. Remarkably, Dr. Berenson, three decades ago, began describing racial and gender differences in cardiovascular risk and pointing to the critical influence of long-term lifestyle trends, such as obesity and smoking. We all owe a tremendous debt to Dr. Berenson for bringing these distributing trends into focus and clarifying the complex interactions of genetics and environment in disease development.  Our national emphasis on healthier children’s diets and lifestyles is to a large extent predicated on the lessons learned from a lifetime of robust research by this extraordinary clinician-scientist.

Dr. Berenson began his enormously productive academic career at Tulane University School of Medicine in 1948, as an assistant in the Department of Medicine. He had received his M.D. degree at Tulane in 1945 and joined his alma mater after service in the U.S. Navy. After four years of clinical and research training with Dr. George Burch and a two-year fellowship with Dr. Albert Dorfman at the University of Chicago, he moved to the faculty of Louisiana State University School of Medicine in 1954. He served with distinction there until 1991, when he rejoined Tulane.  Currently, he is director of Tulane Center for Cardiovascular Health, and Principal Investigator at Bogalusa Heart Study. As Director of NIH funded Specialized Center of Research for Arteriosclerosis and later National Research and Demonstration Center, Dr. Berenson led the Bogalusa Heart Study for the past 34 years. He has published more than 850 journal articles and four books documenting his research.

As you might expect, in view of his distinguished record, Gerald Berenson accumulated a trophy case full of awards and honors. To cite a few of his most recent kudos, he was the initial recipient in 1997 of the Kids First Award of New Orleans Council for Young Children. Tulane honored him with its Outstanding Alumnus Award in 1999 and a Tulane 50th anniversary Lifetime Achievement Award in 1995.  In 2005 he received the Meritorious Achievement Award of the American Heart Association for his contributions to understanding the early origins of atherosclerosis in childhood, and in 2006 he was the recipient of the American Heart Association’s Population Research Prize.

Dr. Berenson has ably served many AHA components, such as the Council on Arteriosclerosis, Thrombosis and Vascular Biology; Epidemiology and Prevention, and the previously mention Cardiovascular Disease in the Young.  He has been an inspirational leader of the association’s Louisiana Affiliate (currently the Greater Southeast Affiliate), of which he was president in 1971.  A widely sought visiting scholar, lecturer and conference leader, Dr. Berenson has ably served many other professional organizations, including the American Society of Hypertension, the American College of Cardiology, and American Society for Preventive Cardiology.  He is a Fellow of the American Association for the Advancement of Science.

Today, Dr. Berenson’s research team has resumed its tasks, but the past few years have been anything but easy. When Hurricane Katrina devastated New Orleans, it also decimated the Tulane School of Medicine. Dr. Berenson lost his home in the storm. He, his wife and labrador were floated out in aluminum bloat boats by sheriff deputies and taken to Baton Rouge. He spent the next four days helping triage patients on the LSU campus and the next six weeks at the Charity Hospital in Baton Rouge. Many of his prized laboratory samples were lost and facilities damaged by wind and rain in Bogalusa.  But even if this acclaimed research had ended forever on that fateful August day – which, fortunately, it did NOT – history would recognize the Bogalusa Heart Study’s achievements as monumental. Now Dr. Berenson and his group are back at work, adding further to an awesome record that fundamentally changed the direction of preventive medicine.

Chief, Division of Cardiovascular Medicine
Director, Institute of Molecular Cardiology
University of Louisville
Louisville, Ky.

After graduating from the University of Perugia (Italy), Dr. Bolli completed a research fellowship at the NHLBI and a clinical cardiology fellowship at Baylor, where he rose to the rank of professor. In 1994, he became chief of cardiology at the University of Louisville. Twice, at two different institutions (Baylor and University of Louisville), Dr. Bolli developed a leading research program.

He has received the ACCP Physician Scientist Award, the Pharmacia-Chiron Young Investigator Award, the NIH MERIT Award, the AHA Basic Research Prize, the Research Achievement Award of the ISHR, the Bowman Research Award (University of Manitoba), the Louis and Artur Lucian Award, the Howard Morgan Award, and the AHA Distinguished Achievement Award. He is a member of the ASCI and AAP and a Foreign Fellow of the Academy of Sciences of the Royal Society of Canada. He has delivered the Keith Reimer Distinguished Lecture of the ISHR, the Robert Berne Distinguished Lecture of the APS, and the George Brown Memorial Lecture of the AHA.

Dr. Bolli has served in the NHLBI Program Project Committee and Advisory Council. Among his AHA activities, he has been a member of the Board of Directors and has chaired the Pathophysiology Review Committee, the Council on Basic Cardiovascular Sciences, and the Council Operations Committee. He was also secretary general and is currently president of the ISHR.  He has served as associate editor of JMCC and is associate editor of Circulation Research and senior guest editor of Circulation.

Dr. Bolli has published 303 papers, including 205 original articles.  Among the original articles, 34 have appeared in Circulation Research, 11 in PNAS, 7 in JCI, and 23 in Circulation.  Thirty-three of his papers have been cited more than 100 times, seven more than 200 times, and five more than 300 times.  He is first or last author in 74 percent of the 205 original articles. His Hirsch factor is 71.

Dr. Bolli’s research has focused on the mechanisms responsible for myocardial ischemia/reperfusion injury and on the development of cardioprotective strategies.  His earlier work established a fundamental role of reactive oxygen species in the pathogenesis of myocardial “stunning,” a concept now accepted as a proven hypothesis.  Subsequently, he identified the signal transduction pathways and cardioprotective genes responsible for the late phase of myocardial “preconditioning,” thereby elucidating the molecular basis of this adaptation of the heart to stress. He is investigating the use of stem/progenitor cells for repair of infarcted myocardium.

Distinguished Professor of Biology and Human Genetics
Investigator,  Howard Hughes Medical Institute
University of Utah School of Medicine
Salt Lake City, Utah

Mario R. Capecchi was born in Verona, Italy in 1937.  He received his B.S. in chemistry and physics from Antioch College in 1961 and his Ph.D. in biophysics from Harvard University in 1967.  He completed his thesis work under the guidance of Dr. James D. Watson.  From 1967-69 he was a Junior Fellow of the Society of Fellows at Harvard University.  In 1969 he became an assistant professor in the Department of Biochemistry, Harvard School of Medicine and was promoted to assocpiate professor in 1971.  In 1973 he joined the faculty at the University of Utah as a professor of biology.  Since 1988 Dr. Capecchi has been an investigator of the Howard Hughes Medical Institute; since 1989, a Professor of Human Genetics at the University of Utah School of Medicine; and since 1993, Distinguished Professor of Human Genetics and Biology.  He is also co-chairman of the Department of Human Genetics.

Dr. Capecchi is best known for pioneering the technology of gene targeting in mouse embryo-derived stem (ES) cells that allows scientists to create mice with mutations in any desired gene by choosing which gene to mutate and how to mutate it.  This gives the investigator virtually complete freedom in manipulating the DNA sequences in the genome of living mice, and allows detailed evaluation of any gene’s function during its development or post-developmental phase.  Research interests include the molecular genetic analysis of early mouse development, neural development in mammals, production of murine models of human genetic diseases, cancer and factors affecting life expectancy, homologous recombination and programmed genomic rearrangements in the mouse.

Dr. Capecchi is a member of the National Academy of Sciences (1991) and the European Academy of Sciences (2002).  His prestigious awards include the Bristol-Myers Squibb Award (1992), Gairdner Foundation International Award (1993), General Motors Corporation’s Alfred P. Sloan Jr. Prize (1994), German Molecular Bioanalytics Prize (1996), Kyoto Prize in Basic Sciences (1996), Baxter Award for Distinguished Research in the Biomedical Sciences (1998), Colby Presidential Endowed Chair (1999), Italian Premio Phoenix-Anni Verdi Award (2000), Spanish Jiménez-Diáz Prize (2001), Albert Lasker Award (2001), National Medal of Science (2001), John Scott Medal Award (2002), Massry Prize (2002), Pezcoller Foundation-AACR International Award for Cancer Research (2003), Wolf Prize in Medicine (2002/03), March of Dimes Prize in Developmental Biology (2005), and the Nobel Prize in Physiology and Medicine (2007) with Oliver Smithies and Martin Evans.

Distinguished University Professor, Northwestern University
SUNY Health Science Center
Brooklyn, N.Y.

Dr. Furchgott was born in Charleston, S.C. He received a B.S. degree in chemistry from the University of North Carolina in 1937 and a Ph.D. degree in biochemistry from Northwestern University in 1940. He was at Cornell University College of Medicine from 1940-49 and at Washington University from 1949-1956. He served as professor and chairman of the Department of Pharmacology at the State University of New York Downstate Medical Center from 1956-1982, and is presently at that institution. Since 1989, he has been adjunct professor of pharmacology at the University of Miami School of Medicine.

His major research interests include cardiac pharmacology, adrenergic peripheral mechanisms, theory of drug-receptor mechanisms, and vascular pharmacology and physiology. Before the advent of radioligands for studying receptors, he developed theory and pharmacological procedures for the characterization of cell-membrane receptors on which drugs, neurotransmitters and hormones act. He was a pioneer in the development of the concept and theoretical basis of “receptor reserve.”

In 1980, Dr. Furchgott reported his discovery of the obligatory role of endothelial cells in the relaxation (vasodilation) of arteries by acetylcholine and related muscarinic agonists. He demonstrated that the relaxation resulted from release of labile factor from the stimulated endothelial cells, a factor he called endothelium-derived relaxing factor or EDRF.

Between 1980 and 1986, discoveries from his laboratory and laboratories worldwide demonstrated that many vasodilators, both endogenous substances and drugs, act by stimulating release of EDRF. Dr. Furchgott independently showed that EDRF acts by stimulating the enzyme guanylate cyclase in vascular smooth muscle cells, leading to an increase in cyclic GMP, which mediates relaxation. He also found that photorelaxation of blood vessels is mediated by an increase in cyclic GMP.

In 1986, Dr. Furchgott had presented evidence for the independent proposal that EDRF is nitric oxide (NO), and that the neurotransmitter released by NANCY (Non-Adrenergic Non-Cholinergic nerves may also be nitric oxide.  The discovery of endothelium-dependent vasodilation and the identification of EDRF as nitric oxide have opened up a new area of research which is contributing much to our understanding of cardiovascular physiology and pathophysiology.

Dr. Furchgott is a recipient of numerous awards and honors; among these are the Goodman and Gilman Award for Research on Receptor Pharmacology from the American Society for Pharmacology and Experimental Therapeutics; the CIBA Award form the AHA’s Council for High Blood Pressure Research; the AHA Research Achievement Award; and the 1998 Nobel Prize in Physiology or Medicine. He is the recipient of numerous honorary doctoral degrees and was the president of the American Society for Pharmacology and Experimental Therapeutics from 1971-72.  He is also a member of the National Academy of Sciences.

James V. Neel Distinguished University Professor of Internal Medicine and Human Genetics
Investigator, Howard Hughes Medical Institute
University of Michigan
Ann Arbor, Mich.

Dr. David Ginsburg is James V. Neel Distinguished University Professor of Internal Medicine and Human Genetics Warner-Lambert/Parke-Davis Professor of Medicine, a member of the Life Sciences Institute at the University of Michigan Medical School, and an investigator at the Howard Hughes Medical Institute.

He received his B.A. degree in molecular biophysics and biochemistry from Yale University and his M.D. degree from Duke University School of Medicine. His postdoctoral clinical and research training was done at the Brigham and Women's Hospital and Children's Hospital, Harvard Medical School.

Dr. Ginsburg is a member of the National Academy of Sciences, the Institute of Medicine, the American Academy of Arts and Sciences, and recipient of the E. Donnall Thomas Lecture and Prize from the American Society of Hematology, the Basic Research Prize from the American Heart Association, and the 2004 ASCI Award from the American Society of Clinical Investigation.

David Ginsburg is interested in understanding the components of the blood-clotting system and how disturbances in their function lead to human bleeding and blood-clotting disorders.

Professor Emeritus of Medicine
Former Director of Cardiovascular Research Institute
University of California, San Francisco
San Francisco, Calif.

Richard J. Havel is known by many as "Mr. Lipoprotein, USA." He, more than any other investigator unraveled the complex metabolism of the plasma lipoproteins beginning with his pioneering work in the Anfinsen lab at the National Heart Institute in Bethesda, Maryland, where he was one of the first Clinical Associates from 1953-1956. His manuscript on the ultracentrifulgal separation of lipoproteins is one of the most frequently cited papers, rivaling Lowry's paper on protein measurement.

He, more than any other investigator, unraveled the complex metabolism of the plasma lipoproteins. He brought order into an area that was at the time murky at best. John Gofinan had made a brave start and insisted on the importance of recognizing the distinctive properties of the several classes of lipoproteins but his analytic ultracentrifugation method was too cumbersome and expensive for widespread clinical use. Nor did it yield quantities of material that would be needed for elucidation of interconversions and catabolic pathways.

Havel introduced a new era when in 1955, while still a Fellow in the laboratory of Christian B. Anfinsen, when he developed preparative ultracentrifugation with his colleagues Howard A. Eder and Joseph H. Bragdon. This technical breakthrough and the series of papers from Havel and others in the NIH group that quickly followed ushered in a new era in the study of lipoprotein metabolism.

Over the ensuing years Havel systematically explored the pathways of lipoprotein catabolism and the metabolic mechanisms controlling it. His synthesis is generally accepted as definitive.

Dr. Havel received his BA form Reed College in Portland, Oregon in 1946, completed his internship a Medicine at New York Hospital (Cornell University Medical School in 1949, and received an M.S. and M.D. Degrees from the University of Oregon Medical School in 1949.  He was Assistant Resident in Medicine, New York Hospital (1950-51), Research Fellow in Medicine, New York Hospital (1951-52), and Chief Resident in Medicine, New York Hospitial (1952-53).

Havel has published over 300 manuscripts. Their quality is attested to by his election to the National Academy of Sciences in 1983; the Institute of Medicine in 1989; the American Academy of Arts and Sciences in 1992. He has received many other honors including the Bristol-Myers Squibb Award for Distinguished Achievement in Nutrition Research and the Distinguished Achievement Award from the AHA Council on Arteriosclerosis.

Distinguished Professor of Pharmacology
UCLA School of Medicine
Beverly Hills, Calif.

Louis J. Ignarro was born in 1941 in Brooklyn, N.Y. and grew up in Long Beach,, N.Y..  He received a B.Sc. degree in Pharmacy/Chemistry from Columbia University in 1962, and a Ph.D. degree in Pharmacology/Physiology from the University of Minnesota in 1966.  He did a postdoctoral fellowship at the N.I.H. in the Laboratory of Chemical Pharmacology in 1966-1968.

Dr. Ignarro’s first research position after training was with the CIBA-Geigy Pharmaceutical Company and in 1973 took on his first academic position at Tulane Medical Center in the Department of Pharmacology.  In 1985, he accepted the position of Professor of Pharmacology at the UCLA School of Medicine, where he remains today.  His current endowed position is the Jerome J. Belzer, MD, Distinguished Professor of Pharmacology.

Dr. Ignarro has received many Awards, most notably: the Basic Research Prize of the American Heart Association; election into the National Academy of Sciences; election into the Academy of Arts and Sciences; election into the American Philosophical Society; and the 1998 Nobel Prize in Physiology or Medicine.

Louis J. Ignarro and two other researchers received the 1998 Nobel Prize in Medicine for their major discoveries involving nitric oxide as a unique signaling molecule in the cardiovascular system.  In 1972, Dr. Ignarro discovered nitric oxide causes vasodilation, lowering of blood pressure, and inhibition of thrombosis.  In 1986, Dr. Ignarro confirmed his suspicion that blood vessels can make nitric oxide, the active ingredient in nitroglycerin, a common drug used to treat heart conditions. Experiments in 1990 showed that nitric oxide is the neurotransmitter responsible for penile erection, and this discovery led to Viagra, the first oral medication for treating erectile dysfunction.

Dr. Ignarro’s discoveries created an explosion of research involving nitric oxide.  In 1986, there were a dozen papers published on nitric oxide and just 10 years later, there were about 7,600 papers.  His observations with nitric oxide have made it possible for medical professionals to understand what protects the cardiovascular system against pathological conditions such as hypertension, stroke, coronary artery disease and other forms of atherosclerosis, gastrointestinal ulcers and vascular complications of diabetes.

Dr. Ignarro’s laboratory at the David Geffen School of Medicine at UCLA has never been larger than eight or nine people.  Throughout his career, funding for the lab has come from the National Institutes of Health (NIH) and local heart associations.  In 2000, Ignarro testified before Congress on the importance of NIH funding for basic science research.  In his testimony, he said that only in America could the son of an uneducated carpenter receive the Nobel Prize in Medicine.

Professor Emeritus, Pharmacology and Biochemistry
University of Washington
Seattle, Wash.

Edwin Gerhard Krebs was born to William Carl Krebs and Louisa Helena StegemanKrebs in Lansing, Iowa, on June 6, 1918. He was the third of four children. His father, a Presbyterian minister, died while Krebs was in his first year of high school. To keep Krebs' two older brothers enrolled at the University of Illinois in Urbana, Louisa Krebs moved the family from Greenville, where Edwin Krebs grew up, to the university town.

In 1940, after completing his high school and undergraduate work in Urbana, Krebs entered medical school at Washington University School of Medicine in St. Louis, Mo. He had the opportunity to work under Arda A. Green, who was associated with Carl Ferdinand Cori and Gerty T. Cori. The Coris were a husband-and-wife team who had won the Nobel Prize in 1947 for research oncarbohydrate metabolism and the enzyme phosphorylase. Krebs' later collaboration with Edmond Fischer at the University of Washington in Seattle had its beginning in the research conducted by the Coris.

After receiving his medical degree in 1943 and completing an eight-month residency in internal medicine at Barnes Hospital in St. Louis, Krebs became a medical officer in the navy, serving in that capacity until 1946. Due to the unavailability of a resident position, and on the advice of one of his professors, Krebs began studying science. Because of his background in chemistry, Krebs chose to work in biochemistry and was accepted by the Coris as a postdoctoral fellow in their laboratory. For two years, while working for the Coris, Krebs studied the interaction of protamine (a basic protein) with rabbit muscle phosphorylase. This work seemed so rewarding to him that he decided to continue his efforts in the field of research, and in 1948 he was invited by Hans Neurath to join the faculty as an assistant professor in the department of biochemistry at the University of Washington.

At this time Neurath's department greatly emphasized protein chemistry and enzymology (enzymes are proteins that act as catalysts in biochemical reactions). Work in the Coris' laboratory had established that the enzyme phosphorylase existed in active and inactive forms, but what controlled its activity wasunknown. Combining his experience on mammalian skeletal muscle phosphorylasewith Edmond Fischer's experience with potato phosphorylase after Fischer joined the department, Krebs and Fischer teamed up to uncover the molecular mechanism by which phosphorylase makes energy available to a contracting muscle. What they discovered was reversible protein phosphorylation. An enzyme calledprotein kinase takes phosphate from adenosine triphosphate (ATP), the supplier of energy to cells, and adds it to inactive phosphorylase, changing the shape of the phosphorylase and consequently switching it on. Another enzyme, called protein phosphatase, reverses this process by removing the phosphate fromphosphorylase, thus deactivating it. Protein kinases are present in all cells.

Once it became evident that reversible protein phosphorylation was a generalprocess, the impact of Krebs and Fischer's work was immeasurable. Their collaboration opened the field of biochemical research and paved the way to much of the work done in the area of biotechnology and genetic engineering. Proteinphosphorylation has even been posited as the basis of learning and memory. Medical applications have included development of the drug cyclosporin, whichblocks the body's immune response by interfering with phosphorylation to prevent rejection of transplants. As important as what happens when the process functions normally is what happens when It goes awry: protein kinases are involved in almost 50 percent of cancer-causing oncogenes.

Recognition for Krebs' work came through various awards besides the Nobel Prize. In 1988 Krebs and Fischer shared the Passano Award for their research, and Krebs was one of four scientists to share the Lasker Award for Basic Medical Research in 1989. He was co-recipient of the Robert A. Welch Award in Chemistry in 1991, followed by the Nobel Prize in physiology or medicine a year later. Besides concentrating his research on protein phosphorylation, Krebs has investigated signal transduction and carbohydrate metabolism.

In 1968 Krebs left the University of Washington to accept the position of founding chairman of the department of biological chemistry at the University of California in Davis. When he returned to Washington in 1977, he became chairman of the department of pharmacology. From 1977 until 1983, Krebs was associated with the Howard Hughes Medical Institute as well.

Besides concentrating his research on protein phosphorylation, Krebs has investigated signal transduction and carbohydrate metabolism.

J.S. Dunn Professor, Regental Professor
Director,  Cell Signaling Center
Institute of Molecular Medicine
University of Texas

Dr. Murad received his M.D. and Ph.D. from Western Reserve University (later Case Western Reserve University) in Cleveland, Ohio, in 1965. In addition to his clinical practice, Murad taught pharmacology at the University of Virginia School of Medicine, Charlottesville (1975-81), Stanford University (1981-89) and  Northwestern University (1988).

While at Stanford, he ventured into the private sector as a vice president of Abbott Laboratories (1988–92) and then became president of the Molecular Geriatrics Corporation (1993-95). He began teaching at the medical school of the University of Texas, Houston, in 1997.

In 1977, Murad showed that nitroglycerin and several related heart drugs induce the formation of nitric oxide and that the colorless, odorless gas acts to increase the diameter of blood vessels in the body. Furchgott and Ignarro built on this work. In 1980, Furchgott demonstrated that cells in the endothelium, or inner lining, of blood vessels produce an unknown signaling molecule, which he named endothelium-derived relaxing factor (EDRF). This molecule signals smooth muscle cells in blood vessel walls to relax, dilating the vessels.

Ignarro's research, conducted in 1986 and done independently of Furchgott's work, identified EDRF as nitric oxide. These discoveries led to the development of the anti-impotence drug sildenafil citrate (Viagra) and had the potential to unlock new approaches for understanding and treating other diseases.

Murad was also the recipient of the Albert Lasker Basic Medical Research Award in 1996 for his discovery. Murad and Ignarro collaborated on Nitric Oxide: Biochemistry, Molecular Biology, and Therapeutic Implications (1995).

Excellence Professor of Pathology and Laboratory Medicine
University of North Carolina at Chapel Hill
Chapel Hill, N.C.

Dr. Oliver Smithies, Excellence Professor of Pathology and Laboratory Medicine at the University of North Carolina at Chapel Hill School of Medicine, shared the 2007 Nobel Prize in physiology or medicine with Mario Cappechi for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells. The achievement marked the pinnacle of a scientific career for Smithies, a UNC faculty member for 19 years, containing numerous honors and two major innovations that have fundamentally changed the science of genetic medicine and laid the foundation for today’s research into gene therapy.  In particular, Dr. Smithies has used gene targeting to develop mouse models for diseases such as cystic fibrosis, thalassemia, hypertension and atherosclerosis.

In the mid-1980s, while at the University of Wisconsin at Madison, Smithies co-discovered a technique to introduce DNA material in cells, replicated a natural process called homologous DNA recombination. He thought that genetic disorders could be treated by correcting mutations in bone marrow cells, or stem cells.  This “gene targeting” led to the creation of transgenic mice, or “designer mice,” that replicated human disease. Smithies’ lab produced the first animal model of cystic fibrosis, a disease caused by one defective gene, and also studied high blood pressure, atherosclerosis and other diseases.

This method also enabled scientists to study specific genes by creating “knock-out mice.” By targeting and removing, or knocking out, a specific gene, researchers can find out what happens when it’s missing. Smithies has used the analogy of removing a steering wheel from a car: without it you soon find out why it has a steering wheel. Now this research method is commonplace in biomedical research and has been the basis for thousands of published papers.

In the 1950s, while at Connaught Medical Research Laboratory in Toronto, Smithies greatly improved gel electrophoresis, a process of separating proteins to identify genes, using starch. The innovation simplified the procedure and became standard in laboratories.

Dr. Smithies’ innovations have revolutionized genetic research and advanced the effective treatment of many diseases, "and millions of people worldwide have better and longer lives because of the talent and determination he has brought to his work,” said UNC chancellor James Moeser. “For decades, he has embodied the very best of academic research and humanity through his modesty, good humor, creativity and love of invention. Through his example, hundreds of students and colleagues have learned how to help the world through research."

Born in 1925 in Yorkshire, England, Smithies as a young child was drawn to the idea of invention and enjoyed building telescopes and radios. He attended a high school for bright students and won a scholarship to Oxford University. He earned a bachelor of arts degree (first-class honors) in physiology from Oxford in 1946, and he went on to earn his master's degree and doctorate in biochemistry from Oxford in 1951.

Professor and Vice Chancellor for Research
University of Colorado, Denver
Aurora, Colo.

Dr. Richard J. Traystman is vice chancellor for research at the University of Colorado Denver. He is also professor of pharmacology at the School of Medicine. He has spent more than 35 years working on the regulation of brain blood vessels, cardiac arrest/cardiopulmonary resuscitation, and stroke.

Dr. Traystman received his B.S. and M.S. degrees from Long Island University in 1963 and 1966, respectively. He received his Ph.D. from Johns Hopkins University Medical Center in 1971 and then did a post-doctoral fellowship at Bowman Gray School of Medicine. He returned to Johns Hopkins Medical Center in 1972 and remained there until 2003 as a Distinguished University Professor. In 2003, he was appointed associate vice president for research planning and development and associate dean for research at Oregon Health Science University.  He was also professor of anesthesiology and peri-operative medicine.

Dr. Traystman has received numerous distinguished awards from both clinical and basic science organizations for his work. He received the Laerdal Prize from the Society of Critical Care Medicine in 1991; the American Society of Anesthesiologists Excellence in Research Award in 1997;  the Robert M. Berne Distinguished Lecturer Award from the Cardiovascular Section of the American Physiological Society in 1996; the Stuart C. Cullen Medal and Distinguished Lectureship Award from the University of California San Francisco in 1998; the Pharmacia-Upjohn Distinguished Lecturer Award from Emory University in 1999; the Hermann Rahn Distinguished Lecturer Award from the State University of New York at Buffalo in 2001; the Society of Critical Care Medicine Excellence in Research Award in 2003; and an honorary doctorate (Sc.D.) from his alma mater, Long Island University, in 1999.

Dr. Traystman has participated in Study Section Review Committees for the National Institutes of Health, American Heart Association and Veteran's Administration. He was associate editor for the American Journal of Physiology: Heart and Circulatory Section, and was deputy editor for Critical Care Medicine. He is presently editor-in-chief of the Journal of Cerebral Blood Flow and Metabolism.

Dr. Traystman also serves on the editorial boards of several other prestigious journals and reviews manuscripts for a multitude of journals. He has served on many AHA committees and has been a stroke fellow for many years. Dr. Traystman has published more than 450 articles in peer-reviewed journals, has trained more than 100 fellows and students, and has been funded by NIH throughout his career.

He is principal investigator of a Program Project Grant from NIH for more than 24 years and has had continuous NIH funding since 1971. Dr. Traystman has been involved in the regulation of the cerebral vasculature and in particular translational research, attempting to translate discoveries from animal, cell, and molecular models to humans with emphasis on normal and pathophysiological states. This work has encompassed the control of cerebral vessels via the nervous system, and hypoxia, to effects of occlusion of cerebral blood vessels (stroke) on brain pathology and neural functional behavior, to pathology resulting from cardiac arrest and cardiopulmonary resuscitation, to neuroprotection with a variety of pharmacological agents and methodologies. He has made major contributions to our understanding of how the brain and its circulation respond to clinical disease states such as stroke and cardiac arrest, and his work is striking for its breadth and application to the adult, neonate, and fetal brain.

Professor of Medicine and Physiology
University of Minnesota
Chief, Section of Cardiology
Veterans Administration Medical Center
Minneapolis, Minn.

Dr. Weir is a professor of medicine and integrative biology and physiology at the University of Minnesota. He was director of cardiac catheterization at the Minneapolis VA Medical Center from 1978 until 1999 and chief of cardiology from 2000 until January 2008.

For more than 35 years, his research has focused on the mechanisms by which oxygen is sensed in the body, particularly hypoxic pulmonary vasoconstriction (HPV), which is important in matching ventilation and perfusion in the lungs, and normoxic contraction of the ductus arteriosus. Failure to contract at birth leads to the common condition of patent ductus arteriosus.

In the 1970s most investigators looked for a vasoconstrictor substance formed during hypoxia that could cause HPV. Dr Weir proposed the alternative concept of "normoxic pulmonary vasodilatation" -- that there is a vasodilator factor active during normoxia. Together, with Dr. Stephen Archer, he developed the hypothesis that changes in oxygen tension alter vascular tone through redox changes in the smooth muscle cells. They were the first to show that hypoxia inhibits potassium channels in the smooth muscle cells of the pulmonary arteries, while normoxia inhibits potassium channels in the ductus. In both cases membrane depolarization and calcium entry follows potassium channel inhibition.

The study of ion channels led to his observation that the anorectic drugs aminorex and dexfenfluramine, which caused outbreaks of pulmonary hypertension, also inhibit voltage-gated potassium channels in pulmonary artery smooth muscle. Subsequent studies in many laboratories have demonstrated the importance of potassium channel function and expression in virtually every animal model of pulmonary hypertension and in idiopathic pulmonary arterial hypertension.

Dr. Weir holds degrees from Oxford University, B.A. (physiology), B.M., BCh. (medical degree) and D.M. (doctorate). He completed his residency/fellowship in internal medicine/cardiology at the Radcliffe Infirmary, Oxford; Hammersmith Hospital, London; and Groote Schuur Hospital, Cape Town, with professors Paul Beeson, John Goodwin and Val Schrire. His research fellowship was at the CVP Laboratory of the University of Colorado, as a Fulbright scholar, under the mentorship of Drs. Jack Reeves and Bob Grover. He is a Fellow of the Royal College of Physicians (London) and received a Fogarty International Fellowship in 1993.

Together, with Dr .Jack Reeves, he initiated the Grover Conferences on the Pulmonary Circulation in 1984, which continue today.  He has been an editor of eleven books on the pulmonary circulation. Between 1999 and 2001 Dr. Weir was chair of the AHA Council on Cardiopulmonary and Critical Care.