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The Endocrine Society |
Citation for the 2004 Fred Conrad Koch Award of The Endocrine Society to Dr. Patricia Donahoe
Patricia Donahoe is a remarkable physician, surgeon, and human being who has made outstanding contributions to endocrinology in her relentless pursuit of the biology of Müllerian-inhibiting substance (MIS). As a surgical resident, she noted that many malignancies were of Müllerian duct origin and made the correlation that the male embryo was capable of completely regressing the Müllerian duct. Based on this observation, she first conceived of and later focused her entire scientific career on the then radical notion of using natural biologic regressors of Müllerian development to inhibit the growth of malignancies of Müllerian origin. She formed these notions long before the term "biologic modifiers" was invented. Her concept of this idea, to which she has clung steadfastly for the past several decades, was well in advance of its time.
One of the most remarkable features of Pat’s career is her fearless acquisition of the appropriate technique for the problem at hand. Initially using her hard-won surgical skills, she pioneered the delicate bioassays using cultivated embryonic genitourinary ridges that were necessary to discern the biologic activities of MIS. Next, she developed the biochemical skills to isolate and sequence MIS, after which she used molecular techniques to clone MIS in collaboration with industrial colleagues. She and her colleagues eventually established their own production facility to ensure sufficient quantities of recombinant MIS to permit unimpeded study of its biological actions and support her growing laboratory team. They next developed the first RIA for MIS, which has now become a standard diagnostic tool in the differential diagnosis of children with ambiguous genitalia and in monitoring malignancies of Müllerian origin, including granulosa cell tumors of the ovary. They subsequently elucidated the structure of the MIS promoters, identified the relevant transcription factors regulating its biosynthesis and secretion, chronicled the detailed developmental pattern of its expression, elucidated its role in the biology of the developing gonad, and cloned and are now studying the MIS receptors and carefully analyzing MIS signaling pathways. Each of these accomplishments would have been sufficient to establish a solid career. As an ensemble, they are nothing short of a tour de force.
In addition to these outstanding scientific achievements, Pat presides over one of the busiest pediatric surgical practices in New England, focusing her attention on abnormalities of the genitourinary system and ambiguous genitalia. On the basis of these contributions, Pat became the first female Professor of Surgery in the history of Harvard Medical School, a member of the National Academy of Sciences, the American Academy of Arts and Sciences, the Institute of Medicine, a fellow of the American Association for the Advancement of Science, and as a Trustee of Boston University. She has also trained a generation of young surgeons and endocrinologists in developmental biology, many of whom now populate Chairs around the world. She has also built a superb pediatric surgical group at the Massachusetts General Hospital that will sustain her commitment to excellence in research, teaching, and patient care well into the future. She has also sustained competitive National Institutes of Health funding for over 30 yr and thus represents a modern paradigm of an able physician/surgeon, an outstanding teacher and mentor, a superb scholar, and an innovative investigator for more than three decades at the Massachusetts General Hospital. There, she has also served on the Institution’s General Executive Committee, Chiefs’ Council, and the Executive Committee on Research, of which she was Chair for 3 yr in the 1980s, following a long line of distinguished investigators.
Balancing these professional roles with those of wife to her invaluable partner and husband Jack, mother to her three children Shauna, Tara, and Jake, and grandmother to her three grandchildren has been done with effortless grace by Pat. Whether it is sailing in Hyannis harbor, wind-surfing or playing tennis in Hyannisport, or hosting quiet dinners for family and friends, Pat handles all with an ease and a warmth that makes all her friends comfortable. For all these achievements, skills, and personal attributes, The Endocrine Society is proud to award Pat Donahoe the 2004 Koch Award, the highest honor of The Endocrine Society.
Walter L. Miller and William F. Crowley, Jr.
Citation for the 2004 Ernst Oppenheimer Award of The Endocrine Society to Dr. Ursula B. Kaiser
Ursula B. Kaiser was born in New Brunswick, Canada, and received her B.Sc. and M.D. from the University of New Brunswick and the University of Toronto, respectively. After completion of a residency in Internal Medicine at St. Michael’s Hospital including a year as Chief Medical Resident, and a clinical fellowship in Endocrinology and Metabolism at Toronto and Mount Sinai Hospitals, she joined me in Boston in 1990 as a Research Fellow in Medicine at the Brigham and Women’s Hospital, Howard Hughes Medical Institute and Harvard Medical School.
Since her work as a fellow and subsequent effort as an independent faculty member at Harvard, working with many important colleagues, including Gwen Childs, Rona Carroll, Dayao Zhao, Andrzej Jakubowiak, Anna Steinberger, David Beier, P. Michael Conn, Constance Albarracin, Gumersindo Fernandez-Vazquez, Lisa Halvorson, Errol Norwitz, Kyeong-Hoon Jeong, Marjorie Zakaria, Gregoy Bedecarrats, and William Crowley, she has become a leader in the field. The key and highly focused goal of Ursula’s research has been an understanding of the molecular and cellular mechanisms of regulation of the pituitary hormones, LH and FSH, particularly by pulsatile GnRH. Clearly, the precise episodic timing of the release of LH and FSH is pivotal for the control of sexual development and reproductive function. The pattern of activation of the genes encoding LH and FSH is determined by the pattern of pulsatile GnRH release and action, but the mechanisms of these effects are poorly understood.
Ursula has identified and characterized the roles of transcription factors Sp1, Egr1, and SF-1 and their interactions in regulating expression of the LHß gene, and of Ptx1 in regulation of the FSHß gene, working toward the goal of identifying the unique transcriptional control mechanisms that allow differential responses to distinct patterns of pulsatile GnRH release. She has elucidated the signal transduction pathways by which pulsatile GnRH mediates these transcriptional responses and has obtained evidence supporting a model wherein GnRH receptor (GnRHR) concentrations are critical in dictating cellular responses to GnRH. Given the important role that she has shown for GnRHR concentrations in dictating these responses, Ursula has also characterized the molecular mechanisms by which GnRHR gene expression is regulated, particularly by GnRH and activin.
Finally, she has applied her knowledge of the cellular mechanisms of GnRH action to better understand the defects in patients with idiopathic hypogonadotropic hypogonadism (IHH). In collaboration with Dr. William Crowley, Jr. at Massachusetts General Hospital, and other investigators internationally, Ursula has identified mutations in the GnRHR gene in patients with IHH, characterized the effects of these mutations on the signal transduction pathways activated by GnRH, and correlated these changes with effects on GnRH-stimulated 
-subunit, LHß, and FSHß gene expression. In this manner, she is identifying and characterizing additional genetic and molecular defects in patients with reproductive disorders, thus allowing a marriage of the bench and the clinic. The elucidation of these mechanisms will improve our understanding of reproductive development, lead to more optimal management of disorders of reproductive function, and assist in the design of therapies for disorders such as fertility, endometriosis, precocious puberty, and prostate cancer.
Ursula joined the faculty at the Brigham and Women’s Hospital and Harvard Medical School as an Instructor in Medicine in 1993, followed by promotion to Assistant Professor of Medicine in 1997 and to Associate Professor of Medicine in 2003. She is also presently Director of the Neuroendocrine Program at the Brigham and Women’s Hospital. She is the recipient of a 1993 Merck Senior Fellows Research Award from The Endocrine Society and the 1995 Women in Endocrinology Janet McArthur Award. In addition, she is a well-regarded physician with expertise in neuroendocrinology, an outstanding teacher with emphasis on undergraduate medical education, a notable mentor and role model, and a remarkable citizen in the academic endocrine world. Finally, on a personal note, Ursula is a wonderfully caring and generous individual who is a devoted wife and mother of two growing boys. In sum, Ursula is most deserving of this accolade that The Endocrine Society has bestowed on her.
William W. Chin
{hd1}Citation for the 2004 Robert H. Williams Distinguished Leadership Award of The Endocrine Society to Dr. David M. de Krester
Professor David de Kretser is recognized internationally as one of the world’s leading reproductive biologists and a major authority on male reproductive endocrinology and fertility. His discoveries have advanced our understanding of one of the most complex systems in all of human biology, with profound implications for clinical care and for the quality of life. He has had a distinguished career as a physician-scientist, educator, and opinion leader from the early days of andrology as a subspecialty to the present day. In addition to his prodigious scholarship, de Kretser has served the wider community through his leadership in academic administration, biotechnology, and bioethics, as well as his mentorship of young scientists.
Educated at the University of Melbourne and Monash University, Professor de Kretser received postdoctoral training with C. Alvin Paulsen at the University of Washington. Professor de Kretser is now the Foundation Director of the Monash Institute of Reproduction and Development at Monash University, as well as Director of the Australian Centre for Excellence in Male Reproductive Health (Andrology Australia). He is Executive Chairman of the Monash Institutes of Health and Chairman of BioMelbourne Network, the leadership forum for the Victorian biotechnology industry.
For more than 30 yr, Professor de Kretser’s research has advanced our understanding of male reproductive physiology and pathology. He defined the ultrastructural features of human spermiogenesis and identified critical defects in spermatozoa of infertile men. He established the existence of paracrine regulatory mechanisms in the testis and continues to explore their action at the molecular level. He codirected work leading to the first isolation of inhibin, one of the most important advances of the past two decades, which has stimulated an explosion of research in male and female aspects of reproduction. He continues to investigate the influence of inhibin, activin, and follistatin in relation to testicular function as well as inflammatory processes, liver disease, and placental physiology. He has illuminated genetic aspects of male infertility and has made important contributions to clinical practice.
Under his leadership, the Monash Institute has made major breakthroughs in the areas of human embryonic stem cells, prostate disease, male and female fertility and infertility, in vitro fertilization, Down syndrome, cancer, and endangered animals.
Five years ago, the Australian government recognized David de Kretser’s prominence by appointing him to direct the new federally funded initiative, Andrology Australia, The Australian Centre for Excellence in Men’s Reproductive Health. The Centre is dedicated to professional and community education as well as collaborative, consolidating research programs.
Professor de Kretser’s contributions have been well recognized by his peers. He is a Fellow of the Royal Australasian College of Physicians, the Australian Academy of Technological Sciences and Engineering, and the Australian Academy of Science. In 2000, he was admitted as an Officer of the Order of Australia in honor of his contributions to medical science. Among many other honors, he received the Distinguished Andrologist Award from the American Society of Andrology in 2003. In 1998 he received an Achiever Award for Advancing Melbourne’s Global Connections. The father of four sons himself, Professor de Kretser was named Victorian Father of the Year for 2001 in recognition of his work in fertility treatment, an honor that he said he shared with the many men he had assisted in becoming parents.
Professor de Kretser has been an active member and leader in national and international scientific societies for three decades. He served as president of the International Society of Andrology, the Australian Society for Reproductive Biology, and the Anatomical Society of Australia & New Zealand. He has been an expert advisor and board member of WHO programs and other international organizations. He has also served on the Bioethics Committee of the Uniting Church in Australia, Victorian Synod.
He has published over 600 papers in international journals and has contributed numerous chapters, reports of meetings and texts relating to male reproductive physiology and medicine. He is the editor of a number of books and has served on the editorial boards of 14 journals. He has supervised more than 50 graduate students and fellows from around the world, including those from 15 developing nations.
David de Kretser’s scholarship, leadership, and dedication to the well being of patients exemplify the pioneering spirit of Robert Williams. This award is a fitting symbol of the high esteem and appreciation of his colleagues and friends around the world.
William J. Bremner and Robert G. Petersdorf
Citation for the 2004 Edwin B. Astwood Award Lecture of The Endocrine Society to Dr. Paolo Sassone-Corsi
Dr. Sassone-Corsi obtained his Ph.D. working on the classical and molecular genetics of the fission yeast Schizosaccharomyces pombe. Subsequently, his interests became centered on the mechanisms governing gene expression in eukaryotes. The strength of his work is found in the application of molecular approaches to physiological questions. In particular, his interests are in understanding how intracellular signaling pathways lead to regulated gene expression in normal and pathological situations, thus uncovering the molecular routes that govern cellular proliferation and tumorigenic growth.
During a post-doctoral period with Pierre Chambon, he developed a system for in vitro eucaryotic transcription and contributed significantly to work that defined the basic structure of promoter regions of genes transcribed by RNA polymerase II. He was the first to show that enhancer sequences were able to stimulate in vitro transcription and demonstrated the involvement of trans-acting factors in their function.
While at The Salk Institute with Inder M. Verma, he worked on nuclear oncogenes, defining how the fos gene is regulated and describing the regulatory function of the Fos protein. He discovered that the expression of the fos gene is under the control of signaling pathways and cellular oncoproteins. He also uncovered an autoregulatory mechanism, the negative feedback loop of the Fos protein on the fos promoter.
In conjunction with his analysis of fos regulation, he participated in the finding that the transcription factor activator protein-1 consisted of the association of Fos with another nuclear oncoprotein, which they also cloned, Jun. These two proteins, when associated, operate in concert to regulate specific early-response genes, an observation that has crucial implications in transcriptional regulation, cellular proliferation, and oncogene cooperation.
Through directed mutagenesis and functional association, his laboratory was the first to define a region, present in both Fos and Jun proteins, which acts as a powerful dimerization domain, the leucine zipper. They also characterized the highly basic region that is required for DNA binding and specific cooperativity between transcription factors. Analysis of the biological properties of Fos and Jun allowed his laboratory to establish a direct link between the activation of specific signaling pathways and the regulation of transcription. This work is seminal and has important implications for the understanding of cellular proliferation as many cellular elements involved in signaling are oncogenic products (i.e. Ras).
Dr. Sassone-Corsi has also contributed to the understanding of the structure, molecular function, and physiology of the transcription factors responsive to cAMP. Indeed, the cAMP-responsive element modulator (CREM) gene was cloned in his laboratory. They have determined the transcriptional regulatory roles played by both cAMP-induced activators and repressors as well as the crucial importance of phosphorylation by various kinases, identifying several examples of signaling cross talk in the nucleus. His group determined that the CREM activator is present in high levels in spermatids and that its activation is a key step in the transcriptional cascade that leads to the regulation of various genes involved in spermiogenesis. Their finding that CREM is not phosphorylated in germ cells led to the discovery of the mechanism for transcriptional activation involving a novel coactivator, activator of CREM in testis (ACT), and its transport by a kinesin. These studies were crucial in the understanding of the molecular events regulating the development of male germ cells.
Dr. Sassone-Corsi and colleagues have also established the importance of negative autoregulatory loops at the transcriptional level as a molecular basis for rhythmic physiological responses. They showed that CREM, which is expressed in a circadian fashion in the pineal gland, is responsible for the circadian oscillation of the hormone melatonin. With experiments in the zebrafish and the mouse, they established the existence of peripheral pacemakers in tissues classically not identified as clock structures.
Modifications occurring at the N-terminal tails of histone molecules are crucial for chromatin remodeling, and Dr. Sassone-Corsi’s laboratory has identified signal transduction routes involved in the phosphorylation of the histone H3 tail in response to growth factors in proliferating cells. He and his colleagues demonstrated that the MAPK-regulated kinase Rsk-2 phosphorylates H3 and results in a local decondensation of chromatin that is directly linked to the activation of early-response genes such as c-fos. During mitosis, the same site is phosphorylated by the kinase Aurora-B, a protein that is highly up-regulated in various human cancers, and results in chromatin condensation.
Dr. Sassone-Corsi has received many awards including the Philips European Award for Young Investigators, the EMBO Gold Medal, the Rosen Prize (Fondation de la Recherche Médicale), the Grand Prix Liliane Bettencourt pour la Recherche, the Segerfalk Lecture Award from Lund University, Sweden, and most recently, the Grand Prix Charles-Léopold Mayer de l’Académie des Sciences for 2003. He was also named as a Member of the European Molecular Biology Organization. For his many and impressive accomplishments, Dr. Paolo Sassone-Corsi is a most worthy winner of the Edwin B. Astwood Award Lecture for 2004.
Douglas M. Stocco
Citation for the 2004 Clinical Investigator Award Lecture of The Endocrine Society to Dr. Shlomo Melmed
Shlomo Melmed, a gold medalist graduate of the University of Cape Town Medical School in 1970, is currently Professor of Medicine and Director of the Cedars-Sinai Research Institute at UCLA, and Chief Academic Officer of the Cedars-Sinai Health System in Los Angeles.
He has made major basic and clinical contributions to understanding pathogenesis, pathophysiology, and therapy of pituitary disease. His pituitary clinical leadership is manifest in leading publications of authoritative practice guidelines and outcomes analyses of pituitary tumor management, coupled with cutting-edge basic pituitary discovery. His fundamental contributions to our knowledge of paracrine pituitary growth factor regulation, mechanisms for pituitary tumorigenesis, and development of peptide analogs for pituitary tumor therapy have immeasurably advanced our knowledge of normal and disordered pituitary function.
He has investigated the role of paracrine soluble factors in determining pituitary function and development. He began by unraveling molecular mechanisms underlying IGF-I feedback signaling in the somatotroph. Performing in vivo and in vitro structurefunction studies of the somatotroph IGF-I receptor, he elucidated mechanisms subserving paracrine regulation of GH transcription. He then demonstrated that overexpressed pituitary-targeted gp130 cytokines regulate Rathke’s pouch development and induce Lhx3-independent pituitary lineages. Building on these observations, he established a novel transgenic model for cytokine-induced Cushing’s disease and also used zebrafish to further our understanding of proopiomelanocortin development and defined the role of cytokine-mediated signal transducer and activation of transcription/suppressor of cytokine signaling-3 autoregulation of proopiomelanocortin transcription and ACTH secretion. These studies provide the molecular basis for the neuro-immune-neuroendocrine interface, and especially the pivotal role of suppressor of cytokine signaling-3 as a critical intrapituitary mediator of ACTH during stress and inflammation. He has recently shown the role of peroxisome proliferator-activated receptor 
receptors in corticotroph cell regulation, which now portends a new area of pituitary investigation.
Since his classic description of ectopic GH secretion causing acromegaly, and culminating 20 yr of studying pituitary adenoma pathogenesis, his laboratory determined the clonal origin of pituitary adenomas and isolated a novel pituitary tumor-derived transforming gene (PTTG). He has linked PTTG expression to pituitary growth factor induction, pituicyte transformation, and adenoma formation. PTTG is the index mammalian securin critical for chromosomal stability and cell cycle regulation. He defined PTTG expression in other neoplasms, and mechanisms for its transcriptional activation. He has shown in vitro and in transgenic models that PTTG overexpression or deletion leads to inappropriate sister chromatid separation, aneuploidy, and defective endocrine cell proliferation. His landmark papers show a mechanism for estrogen-induced pituitary tumors by PTTG and supports the role of antiestrogens in prolactinoma cell control. PTTG discovery has spawned a new focus of investigation for human endocrine cell growth and neoplasia, whereby chromosomal instability associated with PTTG overexpression leads to endocrine cell aneuploidy.
As a clinical leader, he is the senior author on the authoritative guidelines for managing patients with acromegaly. He pioneered the underlying hypotheses for enhancing pituitary tumor therapy by receptor subtype-specific somatostatin analogs now in development for investigator-initiated clinical trials. He showed that combinations of subtype selective somatostatin and dopaminergic receptor ligands uniquely regulate either GH or PRL secretion, and that selective somatostatin receptor-5 activation enhances both somatostatin receptor-2 and dopaminergic efficacy for treating prolactinomas and GH cell adenomas.
Dr. Melmed has had an enduring impact on the education and scientific leadership of pituitary investigation and clinical practice. He is Neuroendocrine Section Editor for the major texts including Williams, and DeGroot and Jameson textbooks of endocrinology, authors the classic textbook of pituitary medicine, The Pituitary, and is founding Editor-in-Chief of the journal, Pituitary. He is past President of the Pituitary Society, past Editor-in-Chief of Endocrinology, Endocrine Society Councilor, served on Endocrinology Study Section, is Program Chair for the 2004 International Congress of Endocrinology, and recipient of both the Pituitary Society Award for Advances in Understanding Pituitary Disease and the Royal Society of Medicine Endocrinology Trust Medal. As a founding director of the Association for the Accreditation of Human Research Protection Programs, he is leading development of national standards for voluntary institutional accreditation for human subjects research. He has successfully mentored over 40 young trainees, many of whom now occupy distinguished endocrinology posts worldwide, especially in the area of pituitary investigation.
He has built a renowned Pituitary Center, successfully integrating patient care and support groups, clinical investigation and trials, and basic pituitary research. He has also energetically led major institutional growth at Cedars-Sinai by spearheading building programs, talented nationally recognized recruitments, and highest quality clinical training program development.
His active publication record in the highest quality basic and clinical journals reflects a dual combination of outstanding basic and clinical scholarly creativity underscoring his standing as an international leader of pituitary medicine.
P. Michael Conn
Citation for the 2004 Gerald D. Aurbach Award Lecture of The Endocrine Society to Dr. David Mangelsdorf
Dr. David Mangelsdorf has been a pioneer in the field of molecular endocrinology through his illuminating studies on hormonal signaling through intracellular nuclear receptors. He is the recipient of the 2004 Gerald D. Auerbach award, which honors outstanding contributions to research in endocrinology. Dr. Mangelsdorf is the Doris and Bryan Wildenthal Professor of Pharmacology and an Investigator of the Howard Hughes Medical Institute at the University of Texas Southwestern Medical Center at Dallas.
David’s work has been consistently marked by originality and innovation that has helped to redirect our thinking of lipid regulation of gene expression. Much of the innovation for this work has come from his deliberate choice of nonsteroidal receptors as model systems. His focus over the last 10 yr has included analysis of vitamin A and vitamin D action. Most recently, he had redirected his interest toward the role of nuclear receptors in regulation of lipid metabolism via dietary lipids such as cholesterol and its metabolites. David’s work is marked by enthusiasm for science, a generosity of ideas, and a sense of humor from which no one is immune.
David’s research program is 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 an undergraduate student at Northern Arizona University in Flagstaff and continued as a graduate student at the University of Arizona in Tucson conducting his research in the laboratory of Dr. Mark Haussler in the Department of Biochemistry. David participated in the purification and cloning of the vitamin D receptor (VDR) in 1987, which was co-authored by last year’s recipient of the Ernst Oppenheimer award, Dr. Donald McDonnell. The numerous subsequent studies of the VDR eventually led investigators to the identification of the genetic basis for two important diseases, vitamin D-resistant rickets and osteoporosis. An interesting highlight of his graduate work was the inclusion of his research by NASA as one of the first academic studies to be flown aboard a space shuttle mission, Challenger flight, June 1985.
With this work as a foundation, David joined my laboratory as a postdoctoral fellow at the Salk Institute in La Jolla, CA, where he continued to pursue his interest in nuclear receptor signaling. David (also known as Davo Mango to us) embarked on a wholly independent direction to isolate orphan nuclear receptors that were important in hepatic function. This effort, to explore the implications of the growing orphan nuclear receptor family, led to the discovery of the retinoid X receptor (RXR). Orphan receptors are novel members of the nuclear receptor family for which hormonal ligands are initially unknown. In many ways, David’s discovery and characterization of RXR helped to transform the field by providing a new crucial member of the nuclear receptor superfamily that is both ancient in its origins and key to understanding signaling by nonsteroidal nuclear hormones. Indeed, RXR has come to be known as a central player in the nuclear receptor family by serving as a unique heterodimerization partner of the VDR, thyroid hormone receptor, retinoic acid receptor, and the peroxisome proliferator-activated receptors. His seminal work on RXR led to two critical advances that helped place the orphan receptors in the mainstream of nuclear receptor signaling. The first, in collaboration with Rich Heyman, was the discovery of the vitamin A metabolite, 9-cis retinoic acid, as a natural RXR ligand. This was the first new nuclear hormone to be discovered since aldosterone in 1953. He demonstrated that RXR hormone response elements are comprised of a direct hexameric repeat spaced by one nucleotide (so-called DR-1) and participated in the demonstration that RXR functions as an obligate heterodimer of other nuclear receptors revealing their role as master regulators of multiple endocrine pathways, helping to establish the importance of these receptors in metabolic regulation. This work was key in helping to usher in the era of orphan receptor research. One important consequence of this work has been the use of RXR as a major therapeutic target for the pharmaceutical industry, both for the treatment of diabetes and certain types of cancer.
Since the initial RXR publication, more than 1500 papers have been published on the subject of RXR and its heterodimeric partners; thus, a risky project initiated 15 yr ago is still having its impact felt today.
At UT Southwestern, David began his research effort to systematically characterize orphan nuclear receptors. His first major discovery was the finding that oxysterols are the endogenous ligands for the liver X receptors (LXRs). The ability of LXR to bind cholesterol metabolites suggested that it may serve the long-sought-after mechanism by which the body senses and disposes of excess cholesterol. Given that nuclear receptors function through the activation of target genes, the LXR genetic network became of paramount interest in deciphering a new mechanism of cholesterol homeostasis. In pursuing this question, David was able to identify the ATP-binding cassette transporter (ABC) A1 gene (ABCA1) as a direct LXR target. Because ABCA1 is a reverse cholesterol transporter, it plays a central role in the body’s trafficking of cholesterol. In addition to regulating this cholesterol pump, Mangelsdorf used homologous recombination to target the knockout of the two LXR genes. Indeed, mice deficient in these receptors were extremely sensitive to changes in dietary cholesterol. With this pathway in place, it has become progressively clear that LXR plays similar roles throughout the body to help pump out the cholesterol in the intestine as well as to control its metabolism in the liver. In addition to its role in cholesterol homeostasis, Mangelsdorf, along with colleague Peter Tontonoz at UCLA, demonstrated that LXR can function as an antiinflammatory receptor to modulate and indeed slow the progression of coronary artery disease. This is important because atherosclerosis is driven in part by high circulating levels of low-density lipoproteins, suggesting a potentially broader role for LXR in total body lipid homeostasis. In the liver, the immediate metabolic products of cholesterol are the bile acids that, through their secretion into the intestine, facilitate the solubilization and absorption of dietary lipids and fat soluble vitamins. In pursuit of these observations, David’s research led to the identification of the endogenous ligands and physiologic functions for other metabolically important receptors, in particular, the bile acid receptor known as FXR (farnesoid X receptor) and the VDR. He was able to demonstrate that FXR functions as a high-affinity receptor in the liver to sense the production of bile acids and to control the expression of a broad set of target genes involved in bile acid homeostasis. This includes the metabolic enzymes that convert cholesterol to bile acids, as well as the transporters that shuttle bile acids through the liver into the gall bladder and ultimately to the intestine. Thus, as with LXR, he was able to demonstrate that the bile acid receptor can function as a type of lipid sensor, governing the transcription of a metabolic cascade of other proteins that help to maintain normal homeostasis of the body’s lipids.
In turning "back to the future," David reactivated his interest in the VDR, which formed the original core of his thesis work. David had known for some time that certain types of toxic bile acids, such as lithocholic acid, can be linked to an increased risk for colon cancer. It is also known that vitamin D can serve a protective role in this capacity. Putting these two observations together, David speculated as to whether the VDR itself might serve as a intestinal sensor for toxic bile acids. Indeed, in a remarkable series of recent experiments, he was able to demonstrate that the VDR once thought to be the sole and primary mediator of the action of vitamin D3, is also a selective but highly sensitive bile acid receptor. Together, these studies show a keen mind at work attempting to integrate diverse aspects of body physiology into a common, unifying pathway.
It is clear that the elucidation of nuclear receptor signaling pathways will help to open a variety of avenues for therapeutic exploration and a number of important disease states. Dr. Mangelsdorf is already an inventor on several patents that are licensed to the pharmaceutical industry and that have led to the discovery of several new drugs. One of these drugs, specific for RXR (Targretin), has been approved as an anticancer therapy. There is little doubt that drugs to LXR and FXR will soon be developed that will provide a new arm in the battle against cholesterol. The biological findings of Dr. Mangelsdorf and his colleagues should provide a solid basis for further advances in pharmacology and therapeutics. The impact of his published work is reflected in numerous citations that have been the subject of several high-profile reviews and have been featured in the hot paper section of The Scientist. Those of you who know Davo have all experienced his infectious enthusiasm and the joy he brings to his work. He is genuinely excited about science and his attitude infuses and motivates his laboratory and the people around him. He is also naturally funny and if he wasn’t a scientist, he would probably have been a stand-up comedian. This great sense of humor also informs his work with a sense of playfulness, and it is clear that work is not really an obligation, but rather a place where he wants to be.
It is a great pleasure to honor our friend and colleague Dr. David Mangelsdorf with the 2004 Gerald D. Aurbach Award.
Ronald M. Evans
Citation for the 2004 Sidney H. Ingbar Distinguished Service Award of The Endocrine Society to Dr. Margaret A. Shupnik
The recipient of the 2004 Sidney H. Ingbar Distinguished Service Award is Margaret A. Shupnik, Ph.D. Every professional organization thrives because a few key people provide the energy, vision, and time to drive its mission. For The Endocrine Society, Margaret, better known as Peggy, is one of these individuals. She has served the Society in numerous capacities as a leader, officer, teacher, researcher, and participant in virtually every committee and task force that has shaped our recent history.
Peggy graduated from Penn State University and received her Ph.D. from Wisconsin, where she trained with Jack Gorski and encountered an experience that cemented her interests in ER action. After a postdoctoral fellowship with Armen Tashjian, she joined the Thyroid Unit at the Massachusetts General Hospital, where she initiated a remarkable series of studies of pituitary physiology with Chip Ridgway, Bill Chin, and other members of these dynamic research teams. Together, they made seminal contributions to our understanding of thyroid hormone regulation of the TSH and -ß subunit genes. Peggy’s ability to perform nuclear run-on transcription assays is legendary and revolutionized our thinking about the rapidity of hormone action at the transcriptional level. In 1988, Peggy moved to the University of Virginia, where she is Professor of Medicine and Physiology. Her recent research has focused on ER action in the pituitary and neuroendocrine system, while continuing studies of gonadotropin gene regulation. Her prolific laboratory has been an excellent training ground for rigorous research design and the use of advanced molecular techniques to elucidate pituitary physiology. Peggy has mentored more than 25 postdoctoral fellows and students and nearly all remain in academic positions.
In addition to her high-impact research, Peggy has made been a tireless participant in peer review by devoting time to numerous editorial boards, including Endocrinology, Molecular Endocrinology, and The Journal of Clinical Endocrinology & Metabolism. She has served on numerous National Institutes of Health (NIH) study sections and was chair of Biochemical Endocrinology. She has driven efforts to ensure representation of endocrine researchers as NIH revises its study sections. In addition to The Endocrine Society, Peggy is also active in the American Thyroid Association, Society for the Study of Reproduction, and Federation of American Societies for Experimental Biology. Within The Endocrine Society, Peggy has performed a remarkable variety of educational and leadership roles. She began Society service on the Public Communications committee. Peggy was a core faculty member of the Molecular and Cellular Endocrinology course for many years, where she delivered superb introductory lectures on transcription, RNA processing, and nuclear receptors. She helped bring the Associates Council to fruition and served on Council, where she championed the role of basic scientists and trainees in The Endocrine Society. Most recently, Peggy was elected Secretary-Treasurer in 1998. In this critical role, she orchestrated a new strategic plan that resulted in a roadmap for the next 5 yr and a major revision of Society by-laws and governance structure. As her term ends, the membership of the Society is indebted to Peggy for giving so much of her time and wisdom.
Peggy has been recognized by several awards including the Van Meter award from the American Thyroid Association and the Oppenheimer award from The Endocrine Society. She exudes energy that is channeled into action. Her vision, passion, and logic commands respect and her resonant voice captures attention. The Endocrine Society has been blessed to have her as a leader. For these contributions and more, Peggy Shupnik is most deserving of the Sidney H. Ingbar Distinguished Service Award.
J. Larry Jameson
Citation for the 2004 Roy O. Greep Award Lecture of The Endocrine Society to Dr. Phyllis M. Wise
The Roy O. Greep Award for 2004 is awarded to Dr. Phyllis M. Wise, Dean of the Division of Biological Sciences and Professor of Neurobiology, Physiology, and Behavior at the University of California, Davis. This award is given in recognition of her contributions to our understanding of the role of estrogen in agerelated changes in brain function.
Phyllis M. Wise, Ph.D., received her undergraduate training from Swarthmore College, followed by M.A. and Ph.D. degrees from the University of Michigan. She also pursued postdoctoral training at Michigan and further expanded her research interests in the actions of ovarian steroid hormones. After spending 2 yr at the University of Mexico, she moved to the University of Maryland, where she firmly established her independent research career and rose through the ranks to full Professor. In 1993, she assumed the chair of the Department of Physiology at the University of Kentucky, and then in 2002, she expanded her administrative responsibilities by becoming a Dean at University of California, Davis.
Dr. Wise initially focused her research on characterizing the effects of aging on neuroendocrine control of reproductive function in the rat, by examining changes in hypothalamic neuropeptide and neurotransmitter activities and estrogen receptor (ER) concentrations. Dr. Wise and her co-workers characterized the changes in these substances that are associated with the increase in GnRH secretion at the time of the ovulatory LH surge. Her studies provided important information not only about the regulation of normal reproductive cyclicity, but also about age-related changes in hypothalamic function associated with decline in GnRH secretion and the eventual loss of ovarian cyclicity. Her work highlighted the importance of catecholamines and the adrenergic receptors in the regulation of GnRH neuronal activity. By carefully studying the transition from young- to middle- to old-age, her studies have contributed to our understanding of the role of the brain in reproductive aging that occurs during the menopausal transition in women.
Dr. Wise expanded her studies to look at the nonreproductive effects of estrogen on age-related brain function. Her work has greatly expanded our understanding of the importance of the neurotrophic and neuroprotective actions of estrogen, which play key roles in the plasticity and survival of the adult brain. She has shown that the permanent hypoestrogenic state associated with aging in the female has profound effects on the vulnerability of the brain to injury. The absence of estradiol increases the extent of cell death after stroke-like injury, and treatment with low, physiological doses of estrogen are profoundly neuroprotective. There is one critical result from her studies that has important therapeutic consequences. If the estrogen was administered before the insult, very low doses of estrogen could provide neuroprotection to the ischemic insult. If the estrogen was administered after the insult, large pharmacological doses were required. Also, her laboratory demonstrated that aging differentially affects the various types of ERs in specific brain regions; the ERß form of the receptor was influenced by aging, whereas the ER form continued to be expressed at relatively normal levels in virtually all brain regions examined. More recent studies have shown that part of estrogen’s neuroprotective effects occur by preventing injury-induced down-regulation of antiapoptotic genes, such as Bcl2, thus promoting cell survival. These studies lay the groundwork for therapeutic treatment with low doses of estrogen to provide neuroprotection against brain injury, a treatment regimen that would not include the negative side effects associated with higher doses.
Dr. Wise has been recognized by her colleagues throughout the world for her outstanding body of research. She was awarded Research Career Development and MERIT grants from NIH. She has received numerous awards, including the Nathan W. Shock Award for outstanding research in aging, the Solomon Berson Award from the American Physiological Society, the Robert W. Kleemeier Award from the Gerontological Society of America, the Albert D. and Elizabeth H. Kirwan Memorial Prize, and the FASEB Excellence in Science Award. In addition to service on a number of boards of private foundations and professional societies, she was also chair of the NIH Biochemical Endocrinology Study Section. Finally, Dr. Wise has served as a mentor to numerous students and fellows, many of whom have research careers in the fields of reproductive physiology and neuroscience. Through her work at the university and national level, she provides a very strong role model for new trainees.
Based on this outstanding record of achievement, The Endocrine Society recognizes Phyllis M. Wise as the recipient of the 2004 Roy O. Greep Award.
M. Susan Smith
Citation of the 2004 Distinguished Educator Award of The Endocrine Society to Dr. E. Brad Thompson
Dr. E. Brad Thompson is an internationally renowned scientist in the field of glucocorticoid action and has made numerous advancements in our understanding of the mechanisms of glucocorticoid action, structure-function analyses of the glucocorticoid receptor, genetic diseases of corticoid resistance, and glucocorticoid target gene activation. He has over 250 scientific publications in refereed journals and books and has been recognized by many honors for his scientific accomplishments. Importantly for this award, however, Brad has made major lifelong contributions to science education at many levels, always instilling enthusiasm and encouraging logical habits of clear thinking in his students and colleagues. The success of this approach is substantiated by the large number of scientists currently working at the forefront of endocrinology whose early development was gently—but firmly—molded by Brad.
He began his scientific career at the National Institutes of Health (NIH), where he was Chief of the Gene Expression Section of the Laboratory of Biochemistry, National Cancer Institute. While at NIH, he fostered the scientific development of more than 20 fellows and visiting scientists from the United States and around the world and taught evening classes in the Foundation for Advanced Education in the Sciences school at NIH educating scientists, at courses and symposia, to the potential advantages of using tissue culture methodology for molecular endocrine studies.
Brad moved to the University of Texas Medical Branch at Galveston in 1984, as I. H. Kempner Professor and Chair of Human Biological Chemistry and Genetics. Motivated by a desire to become more involved in medical and graduate school education, he instituted major improvements in undergraduate teaching. His philosophy is deeply rooted in the premise that learning should be tailored to individual requirements, and he currently chairs a committee with that aim at his school.
While at Galveston, Brad has trained and supervised nine Ph.D. (and M.Sc.) degree candidates, 18 non-degree students and residents, 18 postdoctoral fellows, eight visiting faculty and high school teachers, and numerous rotation students. While maintaining this large and productive group of trainees in Galveston, Brad’s dedication and knowledge of education led to his election to many relevant committees, including his current appointment as Chair of the Committee on Education of the American Medical Graduate Departments of Biochemistry.
Importantly, Brad’s commitment to education has extended even beyond the scientific community. His concern for science education in schools led some years ago to the creation of an outreach program in Galveston that has had a considerable success. A desire to disseminate knowledge of endocrinology at the highest levels is also apparent in Brad’s enthusiasm and dedication as an editor. He was the founding editor of Molecular Endocrinology, now one of the most successful endocrine journals in the world. Recently, he has been appointed to the position of Editor-in Chief of Endocrine Reviews. Throughout his career, Brad has fostered educational activities in the same vein as he has carried out his science, with the highest ideals and sense of ethics.
For this outstanding record of accomplishments, Dr. E. Brad Thompson is the recipient of The Endocrine Society’s Distinguished Educator Award for 2004.
Bert W. O’Malley
Citation for the 2004 Distinguished Physician Award of The Endocrine Society to Dr. Edward S. Horton
The Distinguished Physician Award of The Endocrine Society for the year 2004 is bestowed to Dr. Edward S. Horton, M.D. Over his long and illustrious career, Dr. Horton has demonstrated exceptional talents as a clinician and educator in endocrinology at every level from individual patient interactions to group patient education to the training of students, fellows, and allied healthcare personnel in exemplary care and caring of patients with diabetes and other endocrine disorders.
Dr. Horton received his undergraduate education at Dartmouth College and his M.D. from Harvard Medical School. After clinical training at Johns Hopkins and Duke University, he took his first faculty position at the University of Vermont. At that institution, with his demonstrated skills as a clinician, clinical researcher, and teacher, he held many important positions including Program Director of the Clinical Research Center, Director of Endocrinology, Metabolism and Nutrition, Associate Chairman of the Department of Medicine, and eventually Chairman of the Department of Medicine. In 1993, he moved to the Joslin Diabetes Center to become the Medical Director, and at the same time became Head of Endocrinology and Metabolism at the New England Deaconess Hospital and Professor Medicine at Harvard Medical School.
Throughout his entire career, Ed Horton has been the consummate clinician, clinical researcher, and educator. Both at the University of Vermont and at Harvard Medical School, Dr. Horton has been continuously actively engaged in an integrated career of clinical care, clinical research, and the teaching of medical students, fellows, house staff, and faculty. His particular expertise in the integration of exercise, nutrition, and good diabetes management has made him the doctor of choice for many people with diabetes and an active lifestyle, including internationally competitive athletes. Over the same period of time, he has chaired a number of national and international symposia and has played a major role in establishing clinical care guidelines through his work in the American Diabetes Association as Chair of the Committee on Nutritional Guidelines, with the American Society of Clinical Nutrition as Chair for the Committee on Continuing Education, and for The Endocrine Society as a member of the Public Affairs Committee. Indeed, since 1995, Dr. Horton has been a member of the National Diabetes Education Initiative and since 1998 has served as Co-Chair of this group. He has also chaired the Committee on Ambulatory Care Education at the University of Vermont and directed various post-graduate courses for the American Diabetes Association, American Society for Clinical Nutrition, and other societies. He has served as a principal investigator and on the steering committee of many national multicenter clinical trials that have defined our current standards of care, including the important type 2 Diabetes Prevention Program. He has served on the editorial boards of numerous journals, including serving as Associate Editor of Diabetes, Diabetes Care, and Obesity Research and as a member of the editorial boards of the Yearbook of Endocrinology, The Journal of Clinical Endocrinology & Metabolism, and American Journal of Physiology. He has given invited lectures and has served as visiting professor throughout the world.
In recognition of his many achievements, Dr. Horton served as President of the American Society for Clinical Nutrition and of the American Diabetes Association. He has received the Banting Medal for Distinguished Service from the American Diabetes Association, the Robert Herman Award of the American Society of Clinical Nutrition, the Mizuno Award and Lectureship at Nara, Japan, and most importantly, the Outstanding Physician Educator Award of the American Diabetes Association in 1996.
In summary, Ed Horton in his mild and unassuming way has impacted on patients, students, fellows, nutritionists, exercise physiologists, physicians, scientists, and many other groups as a teacher, integrator of biology and medicine, clinical researcher and clinician par excellence. He has truly demonstrated exceptional achievement as a clinician educator in endocrinology and metabolism as recognized by the Distinguished Physician Award of The Endocrine Society.
C. Ronald Khan
Citation for the 2004 Richard E. Weitzman Memorial Award of The Endocrine Society to Dr. Tso-Pang Yao
Having completed his undergraduate training at the National Taiwan University, Dr. Tso-Pang Yao entered the biomedical training program in Biomedical Science at the University of California, San Diego. His Ph.D. thesis, performed under the mentorship of Dr. Ron Evans, explored the evolutionary conservation of the nuclear hormone superfamily by probing the molecular basis of action of the Drosophila molting hormone ecdysone. In a landmark study published in 1992, he demonstrated that the ultraspiracle protein (usp) in Drosophila was both the functional and structural homolog of the vertebrate retinoid X receptor (RXR) protein. This remarkable result caused them to ask whether there existed proteins in Drosophila that could couple with usp much in the same manner as RXR couples with the vitamin D, thyroid, and retinoid acid receptors in vertebrate systems. Indeed, they were able to determine that the ecdysone receptor actually required usp for high-affinity interactions with both ecdysteroids and specific ecdysteroid-responsive sequences within target genes. Thus, like RXR in vertebrate cells, it appeared that usp was a key regulator of nuclear receptor function in Drosophila. These early studies were enlightening with respect to the evolution of nuclear hormone receptor signaling pathways and highlighted the utility of using genetically tractable organisms, like Drosophila, to study the complexities of nuclear hormone receptor signaling pathways. One practical application that has come from this research is the development of ecdysteroid inducible transcription systems in transgenic mice where the expression of transgenes of interest can be regulated by administration of ecdysteroids. This useful system has seen widespread use among investigators in diverse research fields.
The identification in the mid-1990s of nuclear receptor coactivators, like steroid receptor coactivator (SRC)-1, initiated a plethora of studies aimed at understanding the molecular mechanism(s) by which these ligand-dependent transcription factors made contact with and regulated the expression of target genes. Pang contributed to this effort by demonstrating that the nuclear receptor coactivator SRC-1 was a p300-interacting protein. This finding suggested the transcriptional activity of many nuclear receptors were linked to their ability to recruit p300 using SRC-1 as a bridging protein. The full significance of his work was revealed when it was demonstrated by others that SRC-1, p300, and the closely related cAMP response element binding protein-binding protein (CBP) proteins all exhibit histone acetylase activity and when associated with target gene promoters can effect a local decondensation of chromatin. It was clear from Pang’s studies and those from other groups that p300, and its closely related homolog CBP, were key integrators processing many different signaling inputs and dictating subsequent transcriptional responses. In support of this concept, they demonstrated that ablation of even a single copy of p300 in mice was associated with considerable embryonic lethality. This observation of a gene dosage effect supported the idea that this transcription factor was a central player in transcription and that it was likely to be present in limiting amounts in target cells. Furthermore, they made the surprising observation that the transcriptional activity of nuclear receptors, but not all transcription factors, were attenuated in cells derived from p300 null mice. This introduced the concept of coactivator specificity and suggested that although CBP was adequately expressed in these p300 cells, it could not functionally substitute for p300 in this environment.
Pang brought his interest in CBP/p300 to the Department of Pharmacology and Cancer Biology at Duke, where he is currently an Assistant Professor. In what is likely to become a citation classic, his group published a study that demonstrated that CBP/p300, influenced by factors that cause cell stress, was responsible for p53 acetylation and subsequent increases in the stability of this protein. One of the most interesting aspects of the way Pang does science is that rather than focus on a single molecule and define all of its activities, he moves up and down pathways, an approach that has led him in many directions. A case in point is a recent paper from their group that extends their p53/acetylation observations where they show conclusively that MDM2 and the histone deacetylase 1 (HDACI) are major components of a complex that opposes the ability of p300/CBP to acetylate p53. This got his group interested in histone deacetylases and now a major focus of the group has been the identification of processes other than transcription where acetylation has a regulatory function. Although they have made several interesting observations in this regard, the demonstration that HDAC6 can function as a tubulin deacetylase and regulation of its activity by overexpression has a pronounced effect on cell motility are the most intriguing. They have also found that this enzyme is an integral part of the aggresome regulating the clearance of cytotoxic misfolded proteins from the cell.
The path that has led him from p300/CBP to the study of the nontranscriptional activities of HDACs has yielded many fascinating discoveries. Together, these scientific achievements reflect the efforts of a curious, brilliant scientist who has applied exceptional experimental talent to answer key questions in biology. It is not surprising that he has been able to develop an internationally recognized research program that contributes in several highly competitive fields. His success is clearly a product of his drive and his intellect, but it also reflects the research efforts of his well-mentored students and fellows. It is clear that Pang, an outstanding scientist, scholar, research mentor, and colleague, is a deserving recipient of the 2004 Richard E. Weitzman Award.
Donald P. McDonnell
Citation for The Endocrine Society and Pfizer, Inc. International Award for Excellence in Published Clinical Research in The Journal of Clinical Endocrinology & Metabolism
First Prize
"Luteinizing Hormone Pulsatility Is Disrupted at a Threshold of Energy Availability in Regularly Menstruating Women." Vol. 88, No. 1, pp 297–311. Authors: Anne B. Loucks, Jean R. Thuma. Department of Biological Sciences, Ohio University, Athens, Ohio 45701-2979.
Finalist
"A Longer Biological Night in Long Sleepers than in Short Sleepers." Vol. 88, No. 1, pp 26–30. Authors: Daniel Aeschbach, Leo Sher, Teodor T. Postolache, Jeffrey R. Matthews, Michael A. Jackson, and Thomas A. Wehr. Section on Biological Rhythms, Mood and Anxiety Disorders Program (T.T.P., M.A.J., T.A.W.), National Institute of Mental Health, Bethesda, Maryland 20892; Division of Sleep Medicine, Department of Medicine (D.A.), Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115; Department of Psychiatry (L.S.), Columbia University, New York, New York 10032; and Department of Psychiatry and Human Behavior (J.R.M.), University of Texas Medical Branch, Galveston, Texas 77555-0189.
Finalist
"Effect of Growth Hormone (GH) Treatment on Bone in Postpubertal GH-Deficient Patients: A 2-Year Randomized, Controlled, Dose-Ranging Study." Vol. 88, No. 9, pp 4124–4129. Authors: Stephen M. Shalet, Elena Shavrikova, Morris Cromer, Christopher J. Child, Eberhard Keller, Jirina Zapletalova, Thomas Moshang, Werner F. Blum, John J. Chipman, Charmian A. Quigley, and Andrea F. Attanasio. Christie Hospital (S.M.S.), Manchester M20 4BX, United Kingdom; PSI (E.S.) 191119 St. Petersburg, Russia; Eli Lilly & Company (M.C., J.J.C., C.A.Q.), Indianapolis, Indiana 46285; Universität Klinik (E.K.), Leipzig D-04317, Germany; Palacky University Hospital (J.Z.), Olomouc 772 00, Czech Republic; Children’s Hospital (T.M.), Philadelphia, Pennsylvania 19104-4399; Eli Lilly & Company Windlesham (C.J.C.), Surrey GU20 6PH, United Kingdom; Eli Lilly & Company (W.F.B.), Bad Homburg D-61350, Germany; and Sesto Fiorentino (A.F.A.), 50019, Italy.
Finalist
"Defective Activation of Skeletal Muscle and Adipose Tissue Lipolysis in Type 1 Diabetes Mellitus during Hypoglycemia." Vol. 88, No. 4, pp 1503–1511. Authors: Staffan Enoksson, Sonia K. Caprio, Frances Rife, Gerald I. Shulman, William V. Tamborlane, and Robert S. Sherwin. Department of Medicine, Section of Endocrinology (S.E., R.S.S.), Pediatric Endocrinology (S.K.C., W.V.T.), the General Clinical Research Centers (F.R.), and Howard Hughes Medical Institute (G.I.S.), Yale University School of Medicine, New Haven, Connecticut 06510.
Photos of the winners will be available after the annual meeting of The Endocrine Society and will be published in a future issue.
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