Scientists Emeriti

Greti Aguilera, M.D. had a distinguished career at the NICHD, lasting for over 35 years, studying adrenal steroidogenesis and neuroendocrine mechanisms of adaptation to stress.

Dr. Aguilera received her M.D. from the University of Chile in 1968. After graduation, she was awarded a prestigious fellowship to join a clinical/basic research post-graduate program at the University of Chile, in which she received training in clinical and basic endocrinology, later serving as Associate Professor at the Department of Physiology. In 1975, Dr. Aguilera joined the laboratory of Dr. Kevin Catt at NICHD, first as an International Fogarty fellow and then as a Visiting Scientist. In 1984, Dr. Aguilera was appointed as Senior Investigator in NICHD, and in 1989, as Chief of the Section of Endocrine Physiology, a position she held until her retirement in 2014.

Dr. Aguilera’s research sought to establish a basic understanding of the neuroendocrine mechanisms underlying homeostatic regulation during stress with emphasis on the regulation of the components of the hypothalamic pituitary adrenal axis, neurohypophyseal and autonomic systems. Over the years her laboratory made important contributions to the current knowledge on the regulation and the relative roles of corticotropin releasing hormone (CRH) and vasopressin on the HPA axis, and characterization of the properties, signaling-transduction and regulation of the receptors and actions for these peptide hormones. In addition, to determining the role of vasopressin on the stress response, the work identified novel effects of vasopressin as a neuroprotective agent and trophic factor for the pituitary corticotroph. Her most recent work demonstrating that activation of CRH transcription requires the CREB coactivator, Transducer of Regulated CREB activity (TORC), regulated by the protein kinase, salt inducible kinase (SIK), uncovered a missing link in current knowledge of the regulation of CRH transcription. In keeping with the importance of a cyclic AMP responsive element (CRE) in the CRH promoter in the regulation of CRH transcription, Dr. Aguilera and her colleagues demonstrated that HPA axis hyperactivity following early life stress is associated with increased CRH transcription in response to stress, and hypomethylation CRH promoter CRE. In addition, research addressing the mechanisms of pulsatility of glucocorticoid secretion recently demonstrated that each ACTH-induced secretory pulse is associated with induction of steroidogenic proteins transcription.

Dr. Aguilera's contributions to the knowledge of the physiological, cellular and molecular aspects of the neuroendocrine mechanisms of stress adaptation throughout the years have had profound impact in the field.  In 2007, she received the Mortyn Jones Memorial Medal from the British Society of Neuroendocrinology in recognition of her contributions.

Heinrich Westphal, M.D., was formerly Head of the Section on Mammalian Molecular Genetics in what was then the Program in Genomics of Differentiation at the NICHD. 

Dr. Westphal received his M.D. in 1960 in his native Germany.  He then completed his postdoctoral work at Salk Institute in San Diego, CA under Dr. Renato Dulbecco where he was able to detect viral genes, later named oncogenes, in cells that gained cancerous growth properties as a result of exposure to small DNA tumor viruses.  After spending two years as independent researcher at Cold Strong Harbor Tumor Virus Laboratory under Dr. James D. Watson, Dr. Westphal joined NICHD in 1972, where he spent the remainder of his career. 

Dr. Westphal's first experiments at NICHD were directed toward studying complexes of tumor virus messenger RNA and DNA in the electron microscope. His research team was one of three groups to report the first exciting electron micrographs signaling the phenomenon of RNA splicing. Dr. Westphal received the U.S. Senior Scientist Award of the Humboldt Foundation in recognition of this work.

In subsequent years Dr. Westphal's studies on the molecular genetics of cancer shifted from cell cultures to the living organism. His laboratory became one of the first worldwide to master the technique of generating strains of gene-altered mice. Work was initially focused on the very beginnings of cancer in the initial tumor cell from which the disease spreads into the surrounding tissue. By targeting viral oncogenes to the eye lens of transgenic mice, his team was able to show that the state of cell differentiation in this tissue is inversely proportional to the ability of viral oncogenes to produce malignant and invasive tumors.  Following a decade of observations on oncogenesis versus differentiation in the transgenic mouse, the laboratory established a new focus of research, the molecular genetics of development.  Dr. Westphal and his group began to characterize mouse genes that govern pattern formation and organogenesis in the mouse embryo resulting in the elucidation of key genetic events governing pituitary organogenesis, gonad and kidney formation and forebrain development, as well as gene defects responsible for complex human genetic diseases, including holoprosencephaly and Hirschsprung disease.  Most recently, Dr. Westphal incorporated induced pluripotent stem (iPS) cell technology in his research program in an effort to address disease mechanisms of rare childhood disorders and to create the premises of novel drug therapy including Smith-Lemli-Opitz syndrome (SLOS), an autosomal recessive disorder caused by mutations of the 7-dehydrocholesterol reductase (DHCR7) gene which impairs the final step of cholesterol synthesis.

Over his career, Dr. Westphal contributed over 260 publications to the biomedical literature and his innovation of using the Cre/lox technology as a tool for generating conditional gene mutations in the mouse has been widely adopted in the field.