Department of Pharmacology & Toxicology

Norma C. Adragna, Ph.D., Interim Chair

Past Lectures


Earl H. Morris Endowed Lectureship brings Nobel Prize-winner

Oliver SmithiesDr. Oliver Smithies

Nobel Prize-winner Oliver Smithies, D.Phil., Excellence professor of pathology and laboratory medicine at the University of North Carolina at Chapel Hill School of Medicine, was the keynote lecturer at the Earl Morris Symposium on July 10, 2009, at Wright State University.

On October 8, 2007, the Nobel Foundation announced that Smithies, along with Mario R. Capecchi of the University of Utah's Howard Hughes Medical Institute and Sir Martin J. Evans of the United Kingdom, would share the Nobel Prize in Physiology or Medicine. The scientists were selected "for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells."

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

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

According to the Nobel committee, "gene targeting in mice has pervaded all fields of biomedicine. Its impact on the understanding of gene function and its benefits to mankind will continue to increase over many years to come."


About the Morris Lectureship

An endowed lectureship was established by the family of Dr. Mariana Morris, former chair and professor of pharmacology and toxicology, in honor of her grandfather, Dr. Earl H. Morris. The first invited speaker was Suzanne Oparil, M.D., professor of medicine and director of the Vascular Biology and Hypertension Program at the University of Alabama at Birmingham, who came to Wright State in May 2000. In May 2002, the Earl H. Morris Stress Symposium was held with guest speaker Paul Plotsky, Ph.D., of Emory University, who addressed "Early Adverse Experience as a Developmental Risk Factor."

Rodolfo Llinas, M.D., Ph.D., Thomas and Suzanne Murphy professor of neuroscience and chair of the Department of Physiology and Neuroscience at New York University School of Medicine, presented the Earl H. Morris Lecture on Oct. 17, 2004. A world renowned neuroscientist who pioneered important concepts of neural circuitry and communication within the brain, Dr. Llinas presented "The Neurobiology of Consciousness."

Salvador Moncada, M.D., Ph.D., D.Sc., director of The Wolfson Institute for Biomedical Research at the University College London, presented the Earl H. Morris Lecture on June 22, 2005. Professor Salvador Moncada has revolutionized understanding cardiovascular function and pathology through his research on the role of nitric oxide as a signaling molecule. He presented, "Nitric Oxide, Mitochondria and Cell Signaling."


Dr. Earl H. Morris

History of the Morris Lectureship

Dr. Earl H. Morris was born in Bellbrook, Ohio, in 1872 and received his M.D. From the University of Cincinnati Medical School in 1903. The Montgomery County and Ohio State Medical Societies honored him in 1954 for 50 years of medical practice. The annual lecture series was endowed by his son and daughter-in-law, Herbert C. and Marion Morris.

"An avid learner throughout his lifetime, he was keenly interested in medical research and advances in clinical practice," explains his granddaughter, Mariana Morris, Ph.D., professor of pharmacology and toxicology. "This lectureship is a tribute to his lifelong dedication to the science of medicine."


Burroughs Wellcome Fund Visiting Professorship

Established in 1999, the Burroughs Wellcome Fund Visiting Professorship in Basic Medical Sciences was designed to promote interaction between basic and clinical scientists in the area of cardiovascular sciences. The professorship is supported by the Burroughs Wellcome Fund, an independent private foundation established to advance the medical sciences by supporting research and other scientific and educational activities.

Debra I. Diz, Ph.D., professor of surgical sciences in the Hypertension and Vascular Disease Center and Burroughs Wellcome professor of physiology and pharmacology at Wake forest University School of Medicine in North Carolina, served as visiting professor for the Department of Pharmacology and Toxicology and Department of Pediatrics in May 2002.

Her talk on "Aldosterone Blockade: New Insights into Cardiovascular Protection" focused on an important new drug that can be used to treat hypertension and heart failure. She also presented "Brain Angiotensin Peptides and Reflex Regulation of the Circulation," which examined the use of a new rat model which was genetically engineered to secrete large amounts of a hormone that causes hypertension.

Diz earned her bachelor's from Randolph-Macon Woman's College in Lynchburg, Virginia, and a Ph.D. In pharmacology from the University of Tennessee. Her research interests focus on the brain and kidney renal systems that participate in blood pressure regulation. A widely recognized scientist and educator with an extensive research background, her studies have been funded continuously since 1986. She is an active participant on national and international committees for numerous scientific organizations. Diz has published more than 80 articles, and is on the editorial board of the journals Hypertension and General Pharmacology: the Vascular System.


Peter Arvan, Ph.D., M.D., was the Burroughs Wellcome Visiting Professor in May 1999. The title of his lecture was, "Molecular Chaperones that Regulate Export of Secretory Proteins from the Endoplasmic Reticulum: an Important Role in Thyroid Disease." Dr. Arvan focused on a disease that results from misfolding of the protein thyroglobulin in the thyroid. The molecular chaperone BiP is directly involved in preventing movement of proteins from the ER to the Golgi apparatus until the proteins are folded correctly. In this ER storage disease, thyroglobulin builds up in the ER, causing cell death.

Dr. Arvan is an associate professor of medicine in the Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY. He holds a joint appointment as associate professor in the Department of Developmental and Molecular Biology at Albert Einstein. Dr. Arvan received both his M.D. And Ph.D. from Yale University in 1984. He completed a research-residency program in 1988 at Yale, and was a research fellow in the laboratory of Dr. Howard Rasmussen (Section of Endocrinology) Yale University School of Medicine (1985-86). He was also a clinical fellow in Endocrinology at Yale-New Haven Hospital from 1987-88.

Prior to moving to Albert Einstein College in 1996, Dr. Arvan was an associate professor of medicine at Harvard Medical School. He received the Van Meter Award from the American Thyroid Association in 1997. He has served as a reviewer for NIH study sections on endocrinology and on the NSF cell biology study section. He has been a regular journal reviewer for the Journal of Clinical Investigation, Science, New England Journal of Medicine, and Journal of Cell Biology, and serves on the editorial board of the Journal of Biological Chemistry. He has numerous publications in leading journals and is the principal investigator for numerous research grants. Over the past 20 years, Dr. Arvan has established his career around the process of insulin secretion from pancreatic islet cells and thyroid hormone synthesis by thyroid epithelial cells.