In addition to education, and the multitude of avenues and services that The University of Utah Health Sciences Center provides, our faculty and staff conduct, collaborate and initiate research. We advance knowledge through innovative, basic and clinical research and translate our discoveries into applications that help people.
The University of Utah is ranked among the top 30 public research universities in the nation with particular distinctions in medicine and genetics. As a result of our benchmarking research, the university received over $309 million in research and student aid funding from external sources and ranks 15th in the nation for significant awards to faculty for research efforts.
Research in the health sciences spans many fields of study. From genetics, to molecular biology – from biomedical engineering to drug and pharmaceutical research; University of Utah researchers are on the leading edge of the development and enhancement of knowledge in the medical and health sciences.
University of Utah Research
Physical Abuse More Than Doubles a Woman's Risk for Pelvic Adhesions
Gene's Battle with Microbes Promotes Evolutionary Innovation in Humans
People with rotator cuff tears often experience other tendon or nerve problems as well, but it has been unclear whether those associated ailments are influenced by genetics or environment. New research shows strong evidence that those “global” tendinopathies in the shoulders, knees, hips and other areas appear to cluster among blood relatives and spouses of people with torn rotator cuffs, suggesting that both genetic and environmental factors are involved. In a study leveraging de-identified records from the Utah Population Database (UPDB), a storehouse of health and genealogical data on more than 2 million people, and University of Utah Health Care, researchers found that first-degree relatives – parents, siblings, daughters and sons – are almost twice as likely to get global tendon problems or compression neuropathy, a medical condition caused by direct pressure on a single nerve, than people without rotator cuff tears. Second-degree relatives – grandparents, aunts and uncles, nieces and nephews and half-siblings – also face a significantly higher relative risk for developing tendinopathies and compression neuropathies. Even third-degree relatives of people with rotator cuff tears – great-grandparents, great-grandchildren and first cousins – are at a significantly greater risk for getting compression neuropathies and tendinopathies in the hand and/or wrist. While the risk for tendinopathies and compression neuropathy among relatives indicates a genetic connection to rotator cuff tears, the risk for spouses of people with rotator cuff tears is even stronger, signaling that environmental factors also play a role. The records showed that spouses of those with torn rotator cuffs are almost four times more likely to develop global tendinopathies and compression neuropathies, according to the study. The researchers also found that people with rotator cuff tears have the greatest risk of all for getting those aches and pains – ranging from nine to 15 times higher for tendinopathies and compression neuropathies than people without the painful tears.
Zebrafish Findings Offer Explanation for Variability in Signs of Sepsis
When bacteria or other microbes enter the bloodstream they can trigger the activation of numerous host defenses as part of a process known as inflammation. While inflammation can promote the clearance of the invading microbes, it can also cause collateral damage to the body’s own cells and tissues. In extreme cases, the inflammatory pathways used by the body may spiral out of control, resulting in a life-threatening condition known as sepsis that can lead to organ failure and rapid death. Sepsis kills well over 250,000 people each year in the United States and is the most expensive condition to treat in hospitalized patients. Patients with sepsis are especially difficult to manage because the signs and symptoms of the disease can vary greatly between individuals. In patients with sepsis, the infecting microbes are usually viewed as generic triggers of inflammation while the patients themselves are considered the primary variables that affect disease progression and severity. This viewpoint is challenged by new work published in the April issue of the journal mSphere by researchers in the Department of Pathology at the University of Utah School of Medicine. The study shows that variations in just a single bacterial protein known as flagellin can significantly alter levels of inflammation and the progression of sepsis. Much of this work used a novel zebrafish infection model that mimics many of the key aspects of sepsis seen in human patients. A better understanding of how different flagellin variants differentially affect host inflammatory responses may help researchers develop improved diagnostic and therapeutic tools for sepsis and related diseases. Use of the zebrafish sepsis model may also facilitate the discovery of new treatments that can restore balance to out-of-control inflammatory pathways.