"Hearing loss is the most pervasive occupational health problem in the United States today," says Michael J. Brenner, M.D., director of facial plastic and reconstructive surgery and assistant professor of otolaryngology, head and neck surgery.
Dr. Brenner is the principal investigator for a project studying the mechanisms of cochlear oxidative stress injury and strategies to protect hearing. He received a $1.2 million grant from the National Institutes of Health Mentored Clinical Scientist Development Award (K08).
Dr. Brenner will investigate the molecular basis for hearing loss and pilot innovative strategies for hearing protection. The research team has previously shown that the presence of free radicals and reactive oxygen species within the ear can lead to cellular stress and cell injury. The researchers will now study how targeted interference with key biochemical pathways can be used to prevent hearing loss. The research uses innovative therapeutic agents to decrease free radicals and oxidative stress within the ear.
This project will help scientists understand how antibiotics used for treating life-threatening infections can harm hearing and how such injury may be prevented. These approaches may protect hearing by decreasing inflammation and interfering with cell death pathways.
Dr. Brenner is being co-mentored by Dr. Leonard Rybak, Ph.D., professor of otolaryngology-head and neck surgery; Kathleen C.M. Campbell, Ph.D., professor of otolaryngology and director of the division’s audiology research; and Vickram Ramkumar, Ph.D., associate professor of pharmacology. Debashree Mukherjea, Ph.D., assistant professor of surgery at SIU, has extensively collaborated with Dr. Brenner since the inception of this research program.
The award provides up to five years of support to receive mentored training in laboratory-based biomedical or behavioral research. K08 support develops the skills necessary to pursue independent clinical and/or translational research.Torry receives NIH grant to study pregnancy complications
A research group led by Donald S. Torry, Ph.D., has been awarded a three-year federal grant from the National Institute of Child Health and Human Development, a division of the NIH. Results of the study are expected to provide a better understanding of mechanisms for normal vascular function during pregnancy and may suggest new treatment possibilities for preeclampsia and intrauterine growth retardation.
Thousands of women and babies die or get very sick each year from a condition called preeclampsia, a life-threatening disorder that occurs during pregnancy. It is caused by deficient blood supply to the mother’s placenta causing lack of oxygen and nutrients to the baby, thus affecting proper growth. The mother also develops high blood pressure.
The research will study why placental growth factor is not being produced as it is in normal pregnancies, thus restricting the maternal blood vessels. The research will also study how inflammatory processes, which are also common during preeclampsia, contribute to malfunction of the placenta.
Dr. Torry, professor and chair of medical microbiology, immunology and cell biology at SIU, is the principal investigator for the project. Primary collaborator on the project is Dr. Ronald J. Torry, professor and chair of the pharmaceutical, biomedical and administrative sciences department at Drake University in Des Moines, Iowa, and a research team that includes Shrouq Alhajjaj, graduate student; Yue Guan, Ph.D., postdoctoral fellow; Trenae Mann, research technician and Timothy Murphy, graduate student.New therapy may help heal venous leg ulcers
Many patients with venous leg ulcers located between the knee and the ankle find that their wounds do not heal completely with standard care. Impaired circulation and damage to the veins and valves create painful, slow-healing and often reoccurring wounds in more than 2.5 million people in the United States. These wounds are costly to treat and increasingly more common.
A study led by Douglas B. Hood, M.D., associate professor of surgery, compares the effects of a cell-based topical wound spray created by Healthpoint Biotherapuetics called HP802-247 used with compression therapy against standard therapy alone (infection control, primary dressings and application of compression) in achieving complete wound closure over a 12-week treatment period.
"Many people experience financial hardship due to the costs associated with weekly wound management," Dr. Hood says. "This trial gives us access to the latest cell technology while providing wound care to our patients at no cost. In earlier studies, this treatment has proved to significantly enhance healing rates."
Two separate sprays are sequentially sprayed directly on the wound. As the two sprays mix, they form a matrix that allows the cells in the spray to release growth factors into the wound. Living cells in the sprays interact with the patient’s own cells to stimulate wound healing.
Co-investigators in this study are Kim J. Hodgson, M.D., professor and chair of the division of vascular surgery; Don E. Ramsey, M.D., associate professor of surgery; Robert B. McLafferty, M.D., professor of surgery; and Colleen J. Moore, M.D., assistant professor of surgery.
Healthpoint Biotherapuetics is sponsoring the study.Copello studies calcium regulation in heart failure
Julio Copello, Ph.D., associate professor of pharmacology, will conduct the two-year study, titled "Modulation of Ryanodine Receptor-Mediated Calcium Leak in Health and Diseases." The results of the study may lead to the development of more effective drugs that can be targeted to treat cardiovascular disease. The research is funded by the American Heart Association.
Dr. Copello will study calcium abnormalities that possibly lead to heart disease. His research aims to better understand the cause of faulty calcium regulation inside the heart cells found in various diseases including arrhythmia and heart failure.
According to Dr. Copello, calcium is needed inside the cells to make the heart beat for pumping blood to the body. Each time the heart beats, calcium storage compartments allow calcium to move in and out of the heart cell regions. These regions contain contractile proteins that mediate cell contraction (when calcium moves in) and subsequent relaxation (when calcium moves out). Dr. Copello studies the calcium permeable pores or release channels (ryanodine receptors) that move calcium in. The research will examine the mechanism that causes the pores to open and close in synchrony during activity and stay closed during the heart’s resting period.