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The Endocrine Society |
Citation for the 2005 Fred Conrad Koch Award of The Endocrine Society to Dr. William F. Crowley, Jr.
Bill Crowley was born in Meriden, Connecticut in 1943. He attended Holy Cross College and Tufts Medical School and trained in medicine at the Massachusetts General Hospital, where he remained, with the exception of a short sojourn in the United States Navy, for the whole of his career. Early on, influenced by John Potts, Bill embarked upon a career in endocrinology with an emphasis on reproductive endocrinology. His first tasks in this endeavor were to develop reliable assays for sex steroids and gonadotropins. Once this was accomplished, he used these simple but powerful tools to dissect the pathophysiology of a number of disorders of reproduction. He first examined the secretory patterns of LH and FSH in hypogonadotropic men and showed that fertility could be restored with GnRH replacement administered in a pulsatile manner. Exploring the clinical utility of the newly developed GnRH superagonists, he found that, paradoxically, serum gonadotropin concentrations fell rather than rose, leading to the idea of pituitary "desensitization" and the possibility of using this phenomenon as a therapeutic tool in gonadotropin-mediated, or dependent, diseases such as precocious puberty and prostate cancer. Striking success was achieved in both afflictions. Molecular-based studies into the cellular basis of these diseases followed and have led to a better understanding of the roles of the DAX-1, KAL-1, and FGFR-1 genes and, most recently, the GPR54 gene in normal and disordered function of the reproductive axis in men and women. This work continues and promises many more insights into the causes of disordered reproduction and, in parallel, opportunities for rational therapy.
Bill has been a tireless leader in endocrinology, serving The Endocrine Society as chairman of the Annual Meeting Steering Committee in 1990, council member, chairman of the Professional Affairs Committee, and President in 2001. He has been a champion for translational research, serving as Director of Clinical Research at the Massachusetts General Hospital since 1996 and highlighting the need for increased support for translational research at every opportunity.
Bill’s most important contribution to our discipline, however, is the indelible stamp of his personality and attributes of character: a sunny disposition in the toughest of times, a firm belief in the fidelity of mankind, and his example of the powerful effect of hard work and commitment to the betterment of the human condition. This has rubbed off, in some measure, on all of us. He has made things better. I can think of no person more worthy of this prestigious award.
Lynn Loriaux
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Citation for the 2005 Ernst Oppenheimer Award of The Endocrine Society to Dr. Steven A. Kliewer
Dr. Steven A. Kliewer’s first impact to the field of endocrinology was as a postdoctoral fellow with Dr. Ronald Evans, at which time he demonstrated that the retinoid X receptor, RXR, functions as a common heterodimeric partner for many nuclear hormone receptors, including those for vitamin D, thyroid hormones, retinoic acid, and dietary lipids. This work became the paradigm for understanding the molecular basis of hormone-mediated transcriptional signaling through nuclear receptors. Furthermore, it opened the door to an explosion of new research that would be pursued by Steve and others on characterizing the ligands and physiological functions of orphan nuclear receptors. The RXR heterodimer paper was one of the top 10 scientific papers cited in 1992 and remains a seminal paper in the field.
Dr. Kliewer’s scientific discoveries as an independent investigator have been nothing short of spectacular. Working with a stellar group of scientists at GlaxoSmithKline (including long-time colleagues Tim Willson and Jürgen Lehmann), Steve’s contributions have helped to reshape the field of endocrinology, particularly in the area of drug metabolism. This work is summarized below.
A Treatise on Diabetes.
In 1995, Steve’s group was the first to report that thiazolidinediones (TZDs), a class of drugs used to treat type 2 diabetes, functioned as selective PPAR
agonists. The TZDs had been discovered during the 1970s based on their glucose- and lipid-lowering effects in rodent models of diabetes. Two of these drugs, rosiglitazone and pioglitazone, are currently in clinical use. However, their molecular mechanism of action had remained a mystery. The discovery that PPAR is the molecular target for the TZDs provided new insight into the etiology of type 2 diabetes and paved the way for the rational design of new generations of drugs targeted against this disease. In the area of ligand identification, he showed that a variety of endogenous fatty acids, including certain eicosanoids, bind directly to the PPAR subtypes. This work suggested that PPARs might function as generalized fatty acid sensors and regulate gene expression accordingly. To that end, Steve and his colleagues reported that PPAR coordinately regulates a number of genes involved in glucose and lipid homeostasis in adipose, muscle, and liver. This work also revealed that redistribution of free fatty acids among these tissues is a major antidiabetic action of PPAR agonists.
The Homeotics of Xenobiotics.
In 1998, Dr. Kliewer reported the cloning of the pregnane X receptor (PXR) and demonstrated that it serves as a critical regulator of the cytochrome P450, CYP3A. CYP3A plays a central role in the metabolism of numerous drugs and other potentially toxic xenobiotic lipids encountered by the body. In fact, transcription of the CYP3A gene is induced by many of the same drugs that are metabolized by the CYP3A enzyme, including antibiotics, glucocorticoids, antifungals, and the herbal antidepressant St. John’s wort. Coupling the transcription of CYP3A gene with the broad substrate specificity of the CYP3A enzyme is the basis for many important drug-drug interactions. Remarkably, Steve’s work showed that PXR is the receptor that mediates this metabolic cascade. These findings not only explain the molecular basis for many drug-drug interactions, but have also provided a mechanism for screening candidate drug compounds for their ability to induce CYP3A gene expression.
Many Faces of Bile Acid Homeostasis.
In a complementary set of discoveries, Steve and his Glaxo colleagues have also contributed to our understanding of the feed-forward and feed-back mechanisms that maintain bile acid homeostasis. Their group codiscovered 24(S),25-epoxycholesterol as a naturally-occurring agonist for the orphan nuclear receptor LXR and showed that activation of the RXR/LXR heterodimer induces expression of CYP7A1, the rate-limiting enzyme in bile acid synthesis. Steve also participated in the identification of the bile acid receptor, FXR. His lab went on to show that activation of FXR leads to expression of the repressor protein, SHP, which turns off expression of CYP7A1, thereby explaining the long-sought after mechanism by which bile acids feed back and repress their own synthesis.
On a personal note, Steve brings an intensity to his research that is infectious to those around him. Whether you are collaborating or competing with him, he is fun to have as a colleague, and he shares a remarkable honesty and fairness that is often missed in our field. Steve’s success and the style in which he achieves it make him a fitting recipient of this year’s Ernst Oppenheimer Award. The trail of his success has recently led him to the University of Texas Southwestern Medical Center at Dallas, where he is Professor of Molecular Biology and holder of the Nancy B. and Jake L. Hamon Distinguished Chair in Basic Cancer Research.
David J. Mangelsdorf
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Citation for the 2005 Robert H. Williams Distinguished Leadership Award of The Endocrine Society to Dr. Gordon H. Williams
Dr. Gordon H. Williams is an outstandingly qualified recipient of the Robert H. Williams Distinguished Leadership Award of The Endocrine Society for 2005. His contributions cover a wide range of activities—service, science, education, advocacy, and innovation; all are areas is which he has played key leadership roles.
In terms of service to The Society, Dr. Williams has served as a member of Council, as Vice-Chair and Chair of the Clinical Affairs Subcommittee, and as Chair of the Scientific and Educational Programs Committee; most recently, in recognition of his contribution to the renaissance of aldosterone pathophysiology, he delivered an invited Presidential Plenary Lecture at the Annual Meeting in 2003.
His scientific contributions have been to cardiovascular endocrinology in general and to the genetics and pathophysiology of hypertension in particular. His laboratory showed that a subgroup of essential hypertensive patients have a defect in their sodium-status-mediated responses to angiotensin II. This syndrome, of "nonmodulation," includes 25–30% of the population of essential hypertension; is marked by normal renin levels that are outstandingly responsive to converting enzyme inhibition; and is highly heritable, commonly associated with polymorphisms in angiotensinogen, renin, and aldosterone synthase genes in insulin-resistant lean hypertensives.
Subsequently he and his colleagues in Boston, Paris, and Salt Lake City documented the heritability of low renin hypertension, showing that 10% of such patients are homozygous for a particular 
-adducin allele. They identified the genetic underpinnings of the first monozygotic form of hypertension, glucocorticoid-remediable aldosteronism. In another series of studies, they documented that polymorphisms in the plasminogen activator inhibitor type I gene interact with polymorphisms in the genes of the renin-angiotensin system, providing genetic evidence toward explaining the variable risk of cardiovascular disease in hypertension.
Most recently, as noted above, he has returned to aldosterone-related research, at the benchtop and clinical level, to document the deleterious sequelae of inappropriate mineralocorticoid receptor activation in blood vessels and heart, nonclassical target tissues for aldosterone. He and his co-workers have shown in a variety of animal models that inappropriate aldosterone for salt status produces vascular damage in the heart, kidney- and brain; that this effect is not due to hypokalemia and can be blocked by mineralocorticoid receptor blockade but not potassium loading; and that this effect persisted in PAI-1 knockout mice, an important finding exculpating PAI-1 as a mediator of aldosterone-salt cardiovascular damage.
These basic studies have been extended to the clinic to document the role of aldosterone-salt in hypertension and heart failure. As part of the development of eplerenone, a second-generation mineralocorticoid receptor antagonist, Dr. Williams was involved in the design of a series of studies in human essential hypertensives, which documented the beneficial effects of mineralocorticoid receptor blockade on blood pressure, left ventricular hypertrophy, and albuminuria. Simultaneously, he served as Chair of the Scientific Advisory Committee for EPHESUS, the proof-of-principle trial establishing the efficacy of eplerenone in addition to standard of care for improving mortality and morbidity in heart failure after myocardial infarction.
As an educator, Dr. Williams has trained and mentored over 100 students, fellows, and junior faculty; has taught at Harvard in the pathophysiology course, as well as in the Hypertension Center; has served on the Admissions Committee and chaired the Financial Committee; and has developed and continues to direct a Master’s Degree Program in Clinical Research. Outside Harvard, he has been in extraordinary demand as a guest speaker and for grand rounds presentations; particular recognition in this regard has included the Connors Lectureship of the American Heart Association and the Corcoran Lectureship of the Council for High Blood Pressure Research.
Finally, his most outstanding leadership contribution has been as an advocate for and innovator in the area of patient-centered research. He directed a premier general clinical research center for 30 years and was founder/inaugural president of the General Clinical Research Center’s program Directors’ Association, the Association for Patient-Oriented Research, and the Association of Clinical Research Training Program Directors. He chaired the NIH Clinical Research Study Group, whose recommendations served as the basis for the Clinical Research Enhancement Act (2000), and is currently Founder/Director of the Center for Clinical Investigation, Brigham and Women’s Hospital, and inaugural President of the International Aldosterone Conference.
In summary, for his outstanding contribution and shining example across the areas of service, science, education, patient advocacy, and innovation, The Endocrine Society honors Dr. Gordon H. Williams with the Robert H. Williams Award for Distinguished Leadership.
John W. Funder
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Citation for the 2005 Edwin B. Astwood Award Lecture of The Endocrine Society to Dr. Willa A. Hsueh
Willa A. Hsueh, M.D., is Professor of Medicine and Chief of the Division of Endocrinology, Diabetes, and Hypertension at UCLA School of Medicine in Los Angeles, California. Dr. Hsueh received her M.D. cum laude from Ohio State University and performed postgraduate training in Internal Medicine at Johns Hopkins Hospital. She was a clinical fellow in endocrinology at Johns Hopkins Hospital and a research fellow at Stanford University School of Medicine. Her current research interests focus on insulin resistance and mechanisms of cardiovascular disease, nuclear receptors, the renin-angiotensin system, and vascular complications of diabetes mellitus, with the goal of translating observations at the bench to human pathophysiology and prevention of disease. Her group was the first to identify a potentially protective role for ligands to the nuclear receptor, peroxisome proliferator activated receptor (PPAR). in vascular injury and. more recently, in diabetes complications, particularly in regulation of genes that may mediate vascular complications. The PPAR class of therapeutics is emerging as an important strategy in the war against the metabolic syndrome and diabetes. Dr. Hsueh and her colleagues also demonstrated that coronary vascular damage occurs in insulin resistance in the absence of traditional cardiovascular disease risk and may be related to adipokine production and inflammatory changes, all of which are improved by PPAR ligands. Her group has also identified mechanisms of angiotensin II tissue damage in insulin resistance and diabetes and recently reported a novel effect to inhibit reverse cholesterol transport.
Dr. Hsueh is a fellow of the Council for High Blood Pressure Research of the American Heart Association and presented their Arthur Corcoran Memorial Lectureship (2003). She is a member of numerous other professional societies, including the American Society for Clinical Investigation and the American Association of Physicians. She served on the American Board of Internal Medicine, Endocrinology, Metabolism and Diabetes Committee. Dr. Hsueh was listed among The Best Doctors in America in Endocrinology from 1998 through 2004 and has received many awards, including a MERIT Award of the National Institute of Arthritis, Metabolism, and Digestive Diseases and the Harry Goldblatt Award for Cardiovascular Research of the American Heart Association.
Robert M. Carey
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Citation for the 2005 Clinical Investigator Award Lecture of The Endocrine Society to Dr. Paul M. Stewart
Dr. Paul M. Stewart is recognized as an international expert on the "cortisone-to-cortisol shuttle" and the role of 11-ß-hydroxysteroid dehydrogenase in health and disease. He was born in Harrogate, United Kingdom, and received his M.B. Ch.B. at the University of Edinburgh Medical School in 1982. Paul earned his postgraduate, research M.D. degree with distinction and the award of a Gold Medal at the University of Edinburgh in 1989. Dr. Stewart is Professor of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham. He also serves as Associate Dean of Clinical Research at the Medical School, University of Birmingham, and Clinical Service Lead for Endocrinology at University Hospital Birmingham NHS Trust.
His first publication 20 years ago on chronic nicotine ingestion and atrial fibrillation in the British Heart Journal portended his career in the arena of cardiovascular endocrinology. Dr. Stewart has played a pivotal leading role in developing the hypothesis of so-called "prereceptor" hormone metabolism, that is, the activation or inactivation of hormones in peripheral tissues and the application of this unique mechanism to prevalent diseases including obesity and hypertension. Using a combined clinical and laboratory approach, Dr. Stewart has uncovered some of the candidate pathways involved, which have become novel therapeutic targets raising the possibility of newer approaches to treatment. This talented clinical investigator has authored seminal papers related to proof of the underlying hypothesis of prereceptor hormone metabolism, the purification of some of the enzyme pathways involved, the genetic and clinical characterization of kindreds lacking these enzymes, and use of defined human primary culture systems to undertake confirmatory in vitro and in vivo analyses. Dr. Stewart and colleagues have shown that 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD type 2) "inactivates" cortisol by converting it to cortisone, thereby conferring specificity upon the mineralocorticoid receptor. By contrast, 11ß-HSD type 1 functions as a reductase generating active cortisol at a prereceptor level and enhancing glucocorticoid receptor activation. Failure to down-regulate 11ß-HSD type 1 activity in patients with diabetes may potentiate dyslipidemia, insulin resistance, and obesity. Paul has proposed that inhibition of 11ß-HSD type 1 reductase activity in patients with obesity and the metabolic syndrome, as well as in glaucoma and osteoporosis, may prove to be a unique therapeutic target.
Dr. Stewart’s more than 200 publications in the highest-quality medical journals reflect a dual combination of outstanding basic and clinical scholarly creativity. Paul is an accomplished lecturer and can make the most complex pathophysiology meaningful to the clinician and researcher alike. A highly sought-after speaker, he has delivered over 80 visiting professor lectures, sharing his expertise and insights at academic centers throughout the world. He is also an outstanding clinician with expertise extending to the management of pituitary and adrenal disorders, endocrine hypertension, and reproductive medicine.
In addition to supervising an active endocrinology research group, Dr. Stewart has a major commitment to clinical endocrinology both locally with his hospital/university and at the national and international level. He has an exemplary record of service to the academic community wherein a few examples include serving on several MRC and Wellcome Trust panels, as editor of Clinical Endocrinology, and an editorial board member of The Journal of Clinical Endocrinology & Metabolism and Current Opinion in Endocrinology and Metabolism, as well as Clinical Chair of the 2004 Annual Meeting of The Endocrine Society. In 2005 he will assume the role of Secretary General for the International Society of Endocrinology.
Dr. Paul Stewart is an exceedingly worthy recipient of The Endocrine Society’s 2005 Clinical Investigator Award Lecture.
William F. Young, Jr.
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Citation for the 2005 Gerald D. Aurbach Award Lecture of The Endocrine Society to Dr. David R. Clemmons
David Robert Clemmons, M.D. has been chosen as the recipient of The Endocrine Society 2005 Gerald D. Aurbach Award. An internationally renowned clinical investigator, his translational and clinical studies have made a major contribution to endocrinology in understanding IGF-I action. Born in Nashville, Tennessee, David graduated from Davidson College and received his M.D. degree from the University of North Carolina. He developed an enduring interest in somatomedin-C while still a medical student working with Drs. Louis Underwood and Jud Van Wyk, and that interest has been a theme throughout his spectacular career. After graduation from medical school, he ventured north, although briefly, where he was a house officer and fellow in Endocrinology at the Massachusetts General Hospital in Boston. However, he soon returned to the University of North Carolina to continue his work for over 2 decades, where he currently serves as Chairman of the Division of Endocrinology and the Sarah Graham Kenan Professor of Medicine.
His work on IGF-I, which spans his entire career, is notable for many original and definitive studies. Among his many accomplishments, he was the first to report the diagnostic utility of IGF-I as an integrated marker of GH action. His initial study, published in The New England Journal of Medicine,was the landmark study that revolutionized the diagnosis of acromegaly. His work established the clinical utility of IGF-I, and this study remains the gold standard after 25 years. In addition, it opened up a new area of investigation into GH action. He then established that IGF-I was regulated by nutritional factors and led the field in determining the impact of nutritional disorders on the GH/IGF-I axis. Many current concepts regarding the impact of nutrition and nutritional deprivation on neuroendocrine function are based on these pivotal studies. Dr. Clemmons was the first to report that cells other than hepatocytes synthesize IGF-I. This finding laid the groundwork for the development of the autocrine/paracrine theory of IGF-I action, an area currently studied by investigators who are interested in diseases of muscle and neurological degeneration. His work on the metabolic actions of IGF-I has provided new insights into the role of IGF-I in regulating insulin sensitivity. His studies demonstrated that IGF-I could enhance insulin sensitivity in humans with type II diabetes and that IGF-I is important for maintaining insulin sensitivity in normal subjects.
Dr. Clemmons has also received international recognition for his work on the physiology and importance of IGF-I binding proteins. He discovered that a protease releases IGF-I from IGFBP-3 in serum. Furthermore, he was the first to show that an IGFBP could have a positive effect on IGF-I action. This paper received over 2800 citations. His recent studies have focused on the cooperative interaction between IGF-I receptor-based signaling mechanisms and signaling that is mediated through the Vß3 integrin. This receptor is important for endothelial cell and smooth muscle cell function. These findings have demonstrated that, in a whole-animal model, blocking Vß3 integrin activation is sufficient to markedly attenuate IGF-I actions and, more importantly, this results in inhibition of atherosclerosis. His most recent work has focused on the molecular mechanisms by which these integrin/IGF-I receptor interactions enable smooth muscle cells to survive in hyperglycemic states. These studies have shown the activation of the same mechanism gives a smooth muscle cells a proliferative advantage. This may form the basis for understanding how IGF-I accelerates early proliferative atherosclerotic lesion progression in patients with diabetes.
Dr. Clemmons findings are all important, original contributions, which have made a major impact on the field of endocrinology. Few investigators have moved so seamlessly between the laboratory and clinical research. Although many investigators have moved their work from the laboratory into clinical investigation, David has always asked critical clinical questions and returned to the laboratory to seek more fundamental answers. His findings have advanced the field, stood the test of time, and opened up new areas of research with direct clinical implications.
The recipient of numerous awards, he is the respected member of numerous professional societies, scientific advisory boards, and NIH study sections. His national leadership roles are many and include serving as a Council member for The Endocrine Society and President of the Pituitary Society. He has been on numerous editorial boards and served as Editor of Endocrinology from 1993 until 2002. A highly respected and internationally recognized investigator, clinician, and authority in his field, he is most deserving of this award.
Anne Klibanski
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Citation for the 2005 Sidney H. Ingbar Distinguished Service Award of The Endocrine Society to Dr. P. Michael Conn
P. Michael Conn, recipient of the 2005 Sidney H. Ingbar Distinguished Service Award, has provided remarkable service to the field of endocrinology as an editor, patient advocate, and in leadership roles.
While President of The Society, he promoted the development of the Hormone Foundation (http://www.hormone.org/), constituted and served on its first board and, as interim CEO, developed its logo, mission statement, and oversaw development of its first brochure and first public event.
Also during his presidency, he worked with his congressional representative, herself the mother of a diabetic, to promote use of federal dollars for blood sugar testing, a program that was ultimately included in the Clinton budget as a result of the widespread congressional support. His interest in this area catalyzed the development of the National Diabetes Education Program (http://www.ndep.nih.gov/), jointly funded by the National Institutes of Health and Center for Disease Control, on whose first steering committee he served.
While Editor-in-Chief of The Society’s flagship journal, Endocrinology, he set high standards for review and scientific quality, thereby elevating the journal to 13th among biomedical journals—a ranking not enjoyed before or since. Conn was among the first editors to use Faxes and e-mails to speed the processing of manuscripts and an electronic bulletin board to communicate with authors.
To celebrate the 75th anniversary of the journal, he solicited, and then published "Remembrance" articles—a unique collection of manuscripts identifying landmark moments in our discipline’s history, written by the people who were actually there; these were subsequently published as a collection of essays by The Society.
Conn is a tireless editor, producing over 100 books in endocrinology and serving as past editor of Recent Progress in Hormone Research, Endocrinology, The Journal of Clinical Endocrinology & Metabolism, Molecular and Cellular Neurosciences, and Methods in Neurosciences; as acting editor of Endocrine Reviews, he produced the first topical issue of that journal. Currently he is the editor of Endocrine, Methods, Contemporary Endocrinology, and Contemporary Drug Therapy and is editor or co-editor of texts in Pharmacology, Neuroscience, Neuroendocrinology, Endocrinology, and Molecular Endocrinology, as well as the editor of thirteen volumes of the classic series, Methods in Enzymology, on topics ranging from peptides and second messengers to ion channels, confocal microscopy, and MRI/PET imaging.
As a patient advocate he served as a scientific advisor to the Pituitary Tumor Network Association and National Pituitary Tumor Registry. He continues to work with the Publications Committee of the Pituitary Society.
Conn has served on the National Board of Medical Examiners, including two years as chairman of the Reproduction and Endocrinology Committee.
Over nearly 30 years, his laboratory has consistently contributed to our understanding of fundamental endocrine processes at the cellular level. Among these contributions were early studies of peptide receptor and ligand internalization; receptor-receptor oligomerization; calcium, calmodulin, and lipids as messenger molecules; and, most recently, the role of cellular quality control leading to processing of receptor mutants. These most recent observations have led the way to therapeutic approaches to rescue of receptor mutants.
Supporting the humane use of animals in biomedical research, as The Endocrine Society’s representative on the Federation of American Societies for Experimental Biology (FASEB) Board of Directors, he promoted new projects to educate the public on the importance and welfare safeguards for animals in research. Consistent with his commitment to educating the public on the value and care of animals in research, Conn has designated the honorarium associated with this award to be donated to "Americans for Medical Progress" and the "Northwest Association for Biomedical Research;" these organizations have agreed to support student education with these funds.
Tae H. Ji
Citation for the 2005 Roy O. Greep Award Lecture of The Endocrine Society to Dr. Evan R. Simpson
The Roy O. Greep Lecture for 2005 is awarded to Dr. Evan R. Simpson, Director of the Prince Henry’s Institute of Medical Research and Professor of Biochemistry of Monash University, Clayton, Australia. This award is given in recognition of his contributions to our understanding of the biosynthesis of steroid hormones, particularly the biosynthesis of estrogen by characterization of the enzyme, aromatase.
Evan Simpson, Ph.D., graduated in the Department of Biochemistry at the University of Edinburgh. He pursued postdoctoral study with Ronald Estabrook at the Johnson Research Foundation in Philadelphia and subsequently at the University of Texas Southwestern Medical Center in Dallas. After lectureships in Edinburgh and London, he returned to Dallas where he consolidated his independent research career to become a Professor of Biochemistry and Obstetrics and Gynecology and then Associate Director of the Cecil and Ida Green Center for Reproductive Biology Science. In 1997 he moved to Melbourne, Australia, as Head of the Victorian Breast Cancer Research Consortium laboratory at Prince Henry’s Institute of Medical Research, and then in 1999 he became Director of the Institute.
Dr. Simpson’s work has focused on the biochemistry and molecular biology of the P450 steroidogenic enzymes in the adrenal cortex, placenta, and ovary. His early contributions include the first documentation of the role of the cytochrome P450 hemoprotein in cholesterol side chain cleavage and of the importance of the role of side chain cleavage enzyme in the acute adrenal response to ACTH. In Dallas, in collaboration with Michael Waterman, he demonstrated the role of tropic hormones in regulating the expression of genes encoding the steroidogenic P450s in the adrenal cortex and ovary, by cloning and characterizing cDNAs for these genes and their promoters. They defined the relative importance of LDL cholesterol vs. cholesterol synthesized de novo in adrenal cortical cells, ovarian granulosa cells, and placenta. Characterization of the sources of cholesterol was extended to the human fetus, demonstrating the importance of adrenal synthesis of C19 steroids in the homeostasis of fetal plasma LDL.
Dr. Simpson’s laboratory then focused on the biosynthesis of estrogens, particularly in extragonadal sites, including human adipose tissue. They were the first to clone the cDNA for aromatase and to characterize the human aromatase gene, leading to the understanding of tissue-specific promoter usage, critical to subsequent studies showing the importance of extragonadal synthesis of estrogen in males and postmenopausal women.
This led Dr. Simpson’s group to the hypothesis that local synthesis of estrogen plays an important role in breast cancer development and the maintenance of bone mineralization and cognitive function. This has major significance, reflected in recent studies demonstrating the superiority of aromatase inhibitors over estrogen receptor antagonists for therapy of breast cancer. The side-effects resulting from complete inhibition of estrogen synthesis has made the tissue-specific nature of aromatase expression, demonstrated by Dr. Simpson, a key focus of current studies. Dr. Simpson’s group has, in collaboration with clinical investigators, studied aromatase mutations in estrogen-deficient individuals and created a mouse model of estrogen insufficiency, the ArKO mouse. This has been the springboard for an extensive range of studies with colleagues both in North America and countries worldwide on the role of estrogen in males and females. These studies have revealed many new and unexpected roles for estrogens, including roles in male libido and energy homeostasis.
Dr. Simpson has published over 350 peer-reviewed articles and invited reviews and book chapters. He has received numerous awards including the Trans-Atlantic Medal and the Asia and Oceania Medal from the British Society for Endocrinology and the President’s Scientific Achievement Award from the Society for Gynecological Investigation. He served as Chairman of the Organizing Committee for the International Congress of Hormonal Steroids and the International Aromatase Conference. He is an Associate Editor of Endocrine Reviews and is Editor-in-Chief of the Journal of Molecular Endocrinology. He has served The Society as a member, Chairman of the Annual Meeting Steering Committee in 1998, and member of the Meeting and Educational Progress Committees. He served on the NIH Endocrinology Study Section and as Chair of the Department of Defense Breast Cancer Review Panel. Dr. Simpson has provided leadership as Director of Prince Henry’s Institute of Medical Research, the preeminent Endocrinology Research Institution in Australia. He has mentored over 60 Ph.D. students and postdoctoral fellows, many of whom hold senior positions in obstetrics/gynecology and endocrinology worldwide.
Based on this outstanding record of achievement, The Endocrine Society recognizes Evan R. Simpson as the recipient of the 2005 Roy O. Greep Award.
Jock Findlay
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Citation for the 2005 Distinguished Educator Award of The Endocrine Society to Dr. Ernest L. Mazzaferri
Dr. Ernest L. Mazzaferri is a highly respected national and international endocrinologist with expertise in thyroid disease and, more specifically, thyroid cancer and thyroid nodules. He is the consummate academic physician who has successfully balanced medical administration, teaching, research, and patient care by virtue of his passion for all things medical. He has served as a mentor and role model. He has taught medical students, residents, fellows, research associates, and practicing physicians the art and science of general internal medicine, endocrinology, and thyroid research for over 40 years and has done so with distinction. I have personally observed the excellence of his classroom and beside teaching as well as his care for patients.
Dr. Mazzaferri received his M.D. degree in 1962 and completed Internal Medicine residency and Endocrinology training at Ohio State University. He joined the faculty of the Department of Medicine at Ohio State University in 1968 as an Assistant Professor of Medicine and Assistant Director of the Clinical Research Center. He was promoted to Associate Professor in 1973 and to Professor in 1976. He served as the Director of the Division of Endocrinology until 1978 when he became the Chair of Internal Medicine at the University of Nevada Reno. While at the University of Nevada he also served as acting Dean for two years. He returned to Ohio State University in 1984 as Chair of the Department of Internal Medicine and Professor of Medicine and Physiology. He retired in 1999 and became Professor Emeritus at Ohio State University. In 2001, he accepted an appointment as a Clinical Professor at the University of Florida where he actively teaches and practices endocrinology.
Dr. Mazzaferri has been recognized by students, residents, and practicing physicians for his excellence in teaching. He has received teaching awards from Wilford Hall US Air Force Hospital (1972), Ohio State (1974, 1976, 1977), and the University of Nevada (1981). In addition, he has been the recipient of numerous other teaching awards; these include the Ohio Clinician of the year from the American Diabetes Association, Ohio Affiliate; the Paul Starr award of the American Thyroid Association; the Robert Graves Award of the Thyroid Society for Research and Education; the Earl Metz Outstanding Physician Award of the Ohio State Department of Medicine; the Distinguished Clinician Award of the American College of Endocrinology; and a Mastership from the American College of Physicians.
Dr. Mazzaferri has been a member of the American Board of Internal Medicine subspecialty board in Endocrinology, Diabetes, and Metabolism from 1995–2001 and served as Chair of the subspecialty board and a member of the Board of Directors in 2000 and 2001. He currently is President-elect of the American Thyroid Association.
Dr. Mazzaferri served as a member of the Institute of Medicine National Academy of Sciences Panel, which developed clinical practice guidelines on thyroid cancer screening related to radioactive iodine exposure, and he also served as a member of the National Research Council, Commission on Life Sciences, Committee on Exposure of American People to I-131 from Nevada Atomic Tests: Implications for Public Health, and as a member on the Institute of Medicine, National Academy of Sciences Committee on Health Effects Associated with Exposures Experienced During the Gulf War. He has also been a consultant to the National Academy of Sciences on the Hanford Thyroid Disease Study in 1999.
Dr. Mazzaferri has published over 200 peer-reviewed articles and editorials and over 40 reviews, is editor of the textbook Endocrine Tumors, and is Editor-in-Chief of the Year Book of Medicine. He has been on the editorial boards of The Journal of Clinical Endocrinology and Metabolism, Thyroid, and The Endocrinologist.
Dr. Mazzaferri is best recognized for his work in thyroid cancer, having published important articles on the optimal strategies for diagnosis and treatment of this disorder based upon longitudinal observations of a cohort of patients over a period of thirty years. In addition, he and his laboratory associates have also enhanced our understanding of the basic biological mechanisms that cause papillary thyroid cancer in a transgenic model, and he assisted his associate, Dr. Sissy M. Jhiang, in the identification of the human sodium iodide symporter.
During his career, Dr. Mazzaferri has supervised the training of more than 500 interns and residents in internal medicine and more than 50 endocrine fellows. Many of his former trainees have had distinguished careers in academic medicine and many of his former endocrine trainees have become distinguished clinicians.
Robert Kreisberg
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Citation of the 2005 Distinguished Physician Award of The Endocrine Society to Dr. Robert M. Carey
The Endocrine Society is pleased to present the 2005 Distinguished Physician Award to Dr. Robert M. Carey, David A. Harrison III Distinguished Professor of Medicine at the University of Virginia. Bob is one of the world’s foremost clinical endocrinologists and a pioneer in the field of cardiovascular and renal endocrinology.
He is an opinion leader in adrenal disorders and endocrine hypertension. He described the first cases of isolated hypoaldosteronism and ectopic corticotropic-releasing hormone secretion. He characterized suppression of ACTH by cortisol in dexamethasone-nonsuppressible Cushing’s disease and established criteria for diagnosing primary and secondary adrenal insufficiency.
As Head of the Division of Endocrinology and Metabolism at the University of Virginia from 1978–1986, Bob developed the program into one of the best in the United States (currently ranked number 5 by U.S. News and World Report), based on where clinical endocrinologists would refer their toughest cases.
He has mentored a number of endocrinologists that have established successful clinical and/or research careers throughout the world.
His research has contributed enormously to the understanding of hormonal and autocrine control of renal sodium excretion and blood pressure and causes of endocrine hypertension. He first identified and characterized the inhibitory action of dopamine on aldosterone secretion and demonstrated that dopamine D1-like receptor stimulation induces natriuresis in humans, leading to development of fenoldopam as an approved therapeutic agent for hypertensive crisis. Bob first identified and mapped dopamine receptors in the heart and kidney and demonstrated that dopamine produced in renal proximal tubule cells acts as a paracrine substance to inhibit tubule sodium reabsorption. As a result of Bob’s work, the renal dopaminergic system is now regarded as a major paracrine system controlling 50% of basal sodium excretion.
Bob is a leader in the renin-angiotensin field. He and his colleagues first suggested a self-contained renin-angiotensin system within the kidney and demonstrated its importance in control of sodium excretion and blood pressure. This system is now appreciated as a major mediator of tissue damage in hypertension and diabetes. Bob elucidated the cardiovascular protective functions of the angiotensin AT2 receptor mediated by bradykinin, nitric oxide, and cGMP. Bob recently demonstrated a long-sought mechanism of pressure-natriuresis mediated by renal interstitial cGMP.
Bob received his M.D. degree from Vanderbilt University School of Medicine and completed his residency in medicine at The New York Hospital–Cornell Medical Center. He received training from Dr. Grant W. Liddle at Vanderbilt University and Professor Sir W. Stanley Peart at St. Mary’s Hospital Medical School in London.
From 1986 to 2002, Bob served as Dean of the School of Medicine at the University of Virginia. During his tenure, Bob founded departments of health evaluation sciences, neuroscience, emergency medicine, radiation oncology, and physical medicine and rehabilitation. He initiated centers for clinical trials, biomedical ethics, health of societies, clinical cancer, and digestive health, as well as programs in humanities-in-medicine, generalist medicine, and global health. He developed new research centers in cell signaling, structural biology, retrovirology, reproduction, immunology, and cardiovascular sciences. Bob constructed four major new research buildings and a conference center and developed plans and funding for a fifth research building for the School of Medicine. During his tenure, NIH funds quintupled, private fund raising increased from $2.7 to $40 million per year, and 60 endowed professorships were established. The medical school curriculum was totally revamped and modernized. The basic medical sciences, interdisciplinary research centers, and University-wide collaboration in teaching and research were markedly strengthened during his deanship.
Bob has published over 300 scientific articles and four books. He is a member of the Institute of Medicine of the National Academy of Sciences, the Association of American Physicians, and the American Society for Clinical Investigation and was President of the American Clinical and Climatological Association. Bob is past recipient of the Irvine Page-Alva Bradley Lifetime Achievement Award in Hypertension and is currently Chair of the Council for High Blood Pressure Research of the American Heart Association. He has served as a member of the NIH National Advisory Research Resources Council and is a member of the Association of American Medical Colleges Task Force on Clinical Research. He is a Master of the American College of Physicians (ACP) and received a Laureate Award from the ACP Virginia Chapter. He has participated actively in The Endocrine Society, including service as a member of Council and the Hormone Foundation Board of Directors and Chair of the Development Committee. In 2003, Bob received the highest of award the University of Virginia, the Thomas Jefferson Award, for transforming academic medicine in the University. As David A. Harrison III Distinguished Professor of Medicine, Bob is now devoting his time to teaching, clinical care, and research in endocrinology.
John Baxter
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Citation for the 2005 Richard E. Weitzman Memorial Award of The Endocrine Society to Dr. Peter Tontonoz
Dr. Peter Tontonoz is an emerging leader in the field of molecular endocrinology, in which he has focused his research on the role of lipids as physiological signaling molecules and regulators of nuclear receptor function. He is the recipient of the 2005 Richard E. Weitzman Memorial Award, which is to honor an exceptionally promising young clinical or basic investigator in the field of endocrine research. Dr. Tontonoz is Associate Professor of Pathology and Laboratory of Medicine and an Investigator of the Howard Hughes Medical Institute at the University of California, Los Angeles.
Peter’s work has been consistently marked by originality and innovation that has helped to redirect our thinking of the pathways through which long-chain fatty acids and cholesterol regulate complex patterns of gene expression. Much of the innovation for his work has come through his focus on orphan receptors as potential targets for nonsteroidal hormonal lipids. His focus over the last few years has included an analysis of dietary lipids such as cholesterol and fatty acids and how their metabolites, prostaglandins, and certain insulin-sensitizing drugs act as signaling molecules through orphan receptors such as PPAR and LXR. Peter’s work is marked by a concise clarity in defining the problem, a thoughtful approach to address complex molecular and physiological questions, and a generosity of ideas and reagents, sharpened by a keen interest in good food and music.
Peter’s research career has focused on the mechanism of action of nuclear hormone receptors. These receptors orchestrate the body’s response to a myriad of crucial hormones that include steroid hormones, thyroid hormone, and vitamins A and D. His interest in this field began as a graduate student working with Bruce Spiegelman, during which time he identified the fatty acid-activated nuclear receptor PPAR as the master regulator of adipocyte differentiation. This work uncovered a molecular mechanism whereby dietary lipids directly control adipocyte gene expression and development. In collaboration with our group, he also helped to identify prostaglandin J2 and the thiozoladinedione antidiabetic drugs as PPAR ligands and adipogenic regulators.
With this work as a foundation, Peter joined my laboratory as a postdoctoral fellow at the Salk Institute in La Jolla, California, where he continued to pursue his interest in nuclear receptor signaling. Expanding out of the adipocyte, Peter turned his interests to the role of the PPAR signaling pathways in other cell types, particularly that of the macrophage. Together with Laszlo Nagy, Peter outlined a new role for PPAR in cardiovascular biology. In two landmark papers, they showed that oxidized fatty acids present in the vessel wall activate PPAR and thereby promote macrophage scavenging of atherogenic lipoproteins. These studies provided a molecular explanation for foam cell formation and opened the door to the investigation of nuclear receptors as therapeutic targets in cardiovascular disease.
Peter joined the faculty of UCLA in 1999 and was appointed as an investigator of the Howard Hughes Medical Institute in 2000. His initial studies linked PPAR action in macrophages to that of a second nuclear receptor, LXR, and showed that these two receptors cooperate in the control of lipid metabolism. Subsequent work focused specifically on the role of the LXR pathway in macrophages and its relevance to atherosclerosis. Together with Peter Edwards’ lab, Peter’s group showed that LXR promotes cholesterol efflux from macrophages through a pathway that requires the ABCA1 transporter protein and the related target genes apoE, ABCG1, and PLTP. Studies performed in collaboration with Richard Heyman and David Mangelsdorf confirmed the importance of this pathway in vivo, showing that the genetic absence of LXRs predisposes the macrophage to cholesterol accumulation and atherosclerosis. The Tontonoz lab further established the potential therapeutic relevance of this pathway with the discovery that synthetic LXR ligands inhibit lesion development in mice.
In the past 2 years, Peter’s laboratory has uncovered unexpected links between immune and inflammatory signaling pathways and LXRs. Studies published in 2003 revealed that synthetic LXR agonists have significant antiinflammatory activity in addition to their ability to regulate lipid metabolism. These observations suggest that the ability of LXR ligands to inhibit atherosclerosis may result from effects on both lipid metabolism and inflammation. Peter’s group has also shown that bacterial and viral pathogens interfere with macrophage cholesterol metabolism through inhibition of the LXR signaling pathway, highlighting a potential mechanism whereby microbes may influence cardiovascular disease. Most recently, Peter has examined potential roles for nuclear receptors in macrophage innate immune responses. In a study published in Cell in 2004, his group found that LXR-dependent gene expression regulates macrophage survival and function during intracellular bacterial infection through transcriptional control of the antiapoptotic factor SP. Collectively, Peter’s work has advanced our understanding of how lipids regulate gene expression and has positioned nuclear receptors at the crossroads of metabolic and inflammatory signaling in macrophages.
It is clear that the elucidation of the nuclear receptor signaling pathways will help us to open new avenues toward understanding the mechanistic control of metabolism as well as provide a molecular approach to understanding human disease. There is little doubt that the orphan receptors PPAR and LXR will represent important tools in the battle against cholesterol, hyperlipidemia, and insulin resistance. The biological findings emerging from Peter’s work and that of his colleagues will help to provide a basis for further advances in pharmacology and therapeutics. Those of you who know Peter have all experienced his genuine excitement about science, his joy in sharing new ideas and results, and his ability to articulate complex ideas in a thoughtful, concise fashion.
It is a great pleasure to honor a friend and colleague, Dr. Peter Tontonoz, with the 2005 Richard E. Weitzman Award.
Ronald M. Evans
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Citation for The Endocrine Society and Pfizer, Inc. International Award for Excellence in Published Clinical Research in The Journal of Clinical Endocrinology & Metabolism
Finalist Awards
"X-Chromosome Inactivation Patterns and Androgen Receptor Functionality Influence Phenotype and Social Characteristics as well as Pharmacogenetics of Testosterone Therapy in Klinefelter Patients." Vol. 89, No. 12, pp. 6208–6217. Authors: Michael Zitzmann, Marion Depenbusch, Jörg Gromoll, and Eberhard Nieschlag. Institute of Reproductive Medicine, University of Munster, D-48129 Munster, Germany.
"Exogenous Testosterone or Testosterone with Finasteride Increases Bone Mineral Density in Older Men with Low Serum Testosterone." Vol. 89, No. 2, pp. 503–510. Authors: John K. Amory, Nelson B. Watts, Kirk A. Easley, Paul R. Sutton, Bradley D. Anawalt, Alvin M. Matsumoto, William J. Bremner, and J. Lisa Tenover. Departments of Medicine (J.L.T.) and Biostatistics (K.A.E.), Emory University School of Medicine, Rollins School of Public Health, Atlanta, Georgia 30329; Department of Medicine (N.B.W.), University of Cincinnati College of Medicine, Cincinnati, Ohio 45267; and Department of Medicine (J.K.A., P.R.S., B.D.A., A.M.M., W.J.B.), Veterans Affairs-Puget Sound Health Care System (B.D.A. and A.M.M.), and Geriatric Research, Education and Clinical Center (A.M.M.), University of Washington School of Medicine, Seattle, Washington 98195.
"Insulin-Like Growth Factor I Has a Direct Effect on Glucose and Protein Metabolism, But No Effect on Lipid Metabolism in Type 1 Diabetes." Vol. 89, No. 1, pp. 425–432. Authors: Helen L. Simpson, Nicola C. Jackson, Fariba Shojaee-Moradie, Richard H. Jones, David L. Russell-Jones, Peter H. Sönksen, David B. Dunger, and A. Margot Umpleby. Department of Endocrinology and Diabetes, St. Thomas’ Hospital, GKT School of Medicine (H.L.S., N.C.J., F.S.-M., R.H.J., P.H.S., A.M.U.), London, United Kingdom SE1 7EH; Department of Pediatrics, University of Cambridge, Addenbrooke’s Hospital (D.B.D.), Cambridge, United Kingdom CB2 2QQ; and Department of Diabetes and Endocrinology, Royal Surrey County Hospital (D.L.R.-J.), Guildford, Surrey, United Kingdom GU2 5XX.
"The Effects of Vitamin A Deficiency and Vitamin A Supplementation on Thyroid Function in Goitrous Children." Vol. 89, No. 11, pp. 5441–5447. Authors: Michael B. Zimmermann, Rita Wegmüller, Christophe Zeder, Nourredine Chaouki, and Toni Torresani. Human Nutrition Laboratory, Swiss Federal Institute of Technology Zurich (M.B.Z., R.W., C.Z.), CH-8803 Ruschlikon, Switzerland; Ministry of Health (N.C.), Rabat, Agdal-10000 Morocco; and Department of Endocrinology, University Children’s Hospital (T.T.), CH-8032 Zurich, Switzerland.
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