Research

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.

Research Roundup


Physical Abuse More Than Doubles a Woman's Risk for Pelvic Adhesions

Author: Karen C. Schliep, Department of Family and Preventive Medicine
Co Author: Sunni L. Mumford, Eunice Kennedy Shriver National Institute of Child Health & Human Development, Erica B. Johnstone, Department of Obstetrics and Gynecology, C. Matthew Peterson, Department of Obstetrics and Gynecology, Howard T. Sharpe, Department of Obstetrics and Gynecology, Joseph B. Stanford, Department of Family and Preventive Medicine, Zen Chen, Eunice Kennedy Shriver National Institute of Child Health & Human Development, Uba Backonja, University of Washington Department of Biomedical Informatics and Medical Education, Maeve E. Wallace, Tulane University, Mary Amelia Women’s Center, Germaine M. Buck Louis, Eunice Kennedy Shriver National Institute of Child Health & Human Development
Journal: Human Reproduction, June 22, 2016
Date: 07-06-2016
Women with a history of physical abuse face more than twice the risk of developing pelvic adhesions as women with no history of abuse, a new study finds. The research, which included 473 women 18 to 44 years old at surgical centers in Salt Lake City and San Francisco, also found that 43 percent of the women reported having been sexually abused and 39 percent reported experiencing physical abuse. The study found no association between physical or sexual abuse and endometriosis, ovarian cysts or fibroids. The researchers had hypothesized that the higher risk for pelvic adhesions was due to sexually transmitted infections (chlamydia and pelvic inflammation). But an analysis found that preventing and treating such infections would only partly address the problem and that abuse must be stopped to prevent increased risk for pelvic adhesions.

View article in Human Reproduction, June 22, 2016

Gene's Battle with Microbes Promotes Evolutionary Innovation in Humans

Author: Nels C. Elde, assistant professor of human genetics
Co Author: Matthew F. Barber, Ph.D., Zev Kronenberg, Ph.D. , Mark Yandell, Ph.D., professor of human genetics
Journal: PLOS Genetics, May 20, 2016
Date: 05-31-2016
The lactoferrin gene arose in early mammals approximately 160 million years ago, and can still be found in the genomes of humans and other primates. New research shows that lactoferrin, whose original function was to transport nutrient metals such as iron, has undergone “rapid” evolution to develop another role – immune defense against microbes that cause potentially deadly diseases of meningitis, pneumonia and sepsis. University of Utah researchers believe changes in the lactoferrin gene show evidence of an ongoing battle that drives evolutionary innovation as microbes find new ways of infecting humans and lactoferrin evolves to repel the invaders. The study shows that natural selection has acted on lactoferrin over millions of years, suggesting that lactoferrin has played an important role in the evolutionary success of living primates. In fact, differences in the lactoferrin gene still exist in different human populations across the world today. The research also demonstrates how the emergence of a new immune function in a gene, such as the one in lactoferrin, can drastically alter evolutionary conflicts with microbes.

View article in PLOS Genetics, May 20, 2016

Research Lab Website

Author: Robert Z. Tashjian, M.D., associate professor of orthopedics
Co Author: Lisa A. Cannon-Albright, Ph.D., professor of internal medicine, chief of genetic epidemiology, Craig C. Teerlink, Ph.D., professor of internal medicine (genetic epidemiology), James M. Farnham, M.S., genetic epidemiology, Erin K. Granger, MPH
Journal: Orthopaedic Journal of Sports Medicine, April 12, 2016
Date: 05-18-2016

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.    

View article in Orthopaedic Journal of Sports Medicine, April 12, 2016

Zebrafish Findings Offer Explanation for Variability in Signs of Sepsis

Author: Amelia E. Barber, Ph.D., student in the lab of Matthew A. Mulvery, Ph.D.
Co Author: Brittany A. Fleming, Ph.D., student in the lab of Matthew A. Mulvey, Ph.D., Matthew A. Mulvey, Ph.D., professor of pathology
Journal: mSphere
Date: 04-20-2016

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.

View article in mSphere