Harvey B. Pollard, M.D., Ph.D.
Professor and Chair, Department of Anatomy, Physiology & Genetics, USU SOM
The Center for Medical Genomics and Proteomics in the Department has become one of ten academic organizations in the U.S. to win substantial support (12' million dollars) from the NIH for the establishment of a Proteomics Center. This contract has allowed the University to acquire a world-class set of mass spectrometers, as well as support personnel, which form the technical basis for proteomic research in the 21st Century. In terms of NIH funding, this moves the Department into the ranks of the top twenty equivalent Departments in U.S. Medical Schools, and provides this crucial research resource to the entire University. We will all therefore stand to benefit as an institution. The focus of the Center is lung disease, with a special interest in the inflammatory flagship genetic disease of cystic fibrosis. One citizen in 20 carries one copy of the mutant gene for cystic fibrosis, and it is the most common autosomal recessive fatal disease in the U.S. Information derived from the Center promises to impact on our understanding of more challenging, but less understood inflammatory diseases of the lung such as asthma, and inflammatory processes in other parts of the body.
Rosemary C. Borke, Ph. D.
Vice Chair for Instruction, Professor, USU SOM Department of anatomy, Physiology & Genetics
Professor Borke's Course, Clinical Head and Neck and Functional Neuroscience, has been a perennial favorite of the first-year medical students. She has made on-going improvements such as the inclusion of additional educational; materials that stress clinical correlations, demonstrating the importance of a firm grounding in the basic sciences. Professor Borke has also produced compact disks (CDs) for instructional purposes in the classroom, as well as for home study.
Juanita J. Anders, Ph.D., Associate Professor &
Kimberly Byrnes, Ph.D., Department of Anatomy, Physiology and Genetics, USU SOM
Light of specific wavelengths can penetrate to different depths of the body. Through its absorption by a cellular photoreceptor, light can modulate basic cellular functions including energy (ATP) production and DNA, RNA, and protein synthesis. Therefore, light has the potential as a non-invasive therapy for deep tissue repair. Drs. Anders and Byrnes demonstrated that light could increase neuronal survival and regeneration in the injured peripheral nervous system. This work led to a series of experiments on the use of light as a non-invasive treatment for spinal cord injury (SCI). In the United States, approximately 230,000 people live with the effects of SCI and this number increases by 11,000 each year. SCI causes devastating disabilities due to the inability of axons within the central nervous system to regenerate following an injury. While advances in emergency care and rehabilitation allow many SCI patients to survive, methods for reducing the extent of injury and for restoring function are still limited. Drs. Anders and Byrnes, in collaboration with Drs. Waynant and Ilev, colleagues from the Food and Drug Administration, identified that 810nm light could penetrate to the depth of the spinal cord. Light treatment of injured spinal cord with an 810 nm, 150 mW (dosage = 1589 J/cm2) diode laser, acted as an immunosuppressant and improved axonal regeneration and functional recovery. This research suggested that light treatment is a novel and effective treatment for SCI, and in 2003 led to the filing of a Provisional Patent Application and licensing of this technology to PhotoThera, Incorporated.
Sharon L. Juliano, Ph.D.
Professor, Department of Anatomy, Physiology and Genetics, USU SOM
There are numerous disorders of neuronal migration into the neocortex. Impaired migration can lead to human dysfunctions that range from epilepsy to schizophrenia. Factors influencing cortical development and subsequent migration are both genetic and environmental; members of Sharon Juliano's laboratory (Marcin Gierdalski and Sylvie Poluch) have been using both genetic and epigenetic models to obtain better understanding of the impaired mechanisms of neuronal migration. They previously demonstrated that a short interruption of early cortical development during gestation could result in dramatic alterations in radial glial cells, which form an important scaffold for neurons migrating into and forming the cerebral cortex. In collaboration with colleagues from Harvard University, Juliano and Gierdalski determined that a protein of approximately 50 kDa is an endogenous factor in mammalian cortex, which is capable of reorganizing radial glial cells toward their normal morphology. They further established that the likely endogenous factor is neuregulin and that it acts through erbB receptors. The outcome of their studies may clarify both the mechanisms that produce neuronal migration disorders during pregnancy and potential repair of these disorders by systemically investigating the factors involved in several structural and neurochemical elements that contribute to impaired migration. Their findings were published in a special issue of the journal Cerebral Cortex, which commemorated the currant status of research on neocortical development.