A University of Hawaii researcher has received a $104,477 grant to see whether resources from Hawaii waters can be used to ward off sepsis, an often fatal complication of infection.

The National Institutes of Health awarded the grant last month to Felix Ikuomola, a Ph.D. candidate in clinical research at the John A. Burns School of Medicine and a graduate research assistant at the UH Cancer Center. The diversity grant is a supplement to funding provided to Ikuomola’s mentor, UH Cancer Center assistant professor Michelle Matter.

Sepsis shock deprives organs of blood, which can trigger widespread organ failure and death. According to the UH Cancer Center, sepsis kills 30 percent of cancer patients and is the No. 10 cause of death among seniors.

While symptoms of sepsis can be treated by fluids and antibiotics, there is no known prevention or cure for the condition itself.

Ikuomola’s research is based on the understanding of how injury or damage to endothelial cells, which cover the innermost part of blood and lymphatic vessels, can cause widened pores in the vascular lining, which in turn can result in sepsis.

Ikuomola has been screening small molecules, fungi and Hawaii marine natural products to see whether there is a way to block or prevent "leakiness" in endothelial cells.

"We are very hopeful that these Hawaiian marine natural products will work in sepsis because the marine natural products are able to survive the harsh and salty conditions of the ocean and are able to control and regulate their internal conditions," Ikuomola said in a release.

Ikuomola said he hopes to understand how these products regulate their cells so they do not suffer from the sort of excessive permeability that could lead to uncontrolled influx of ocean water or the loss of cellular contents.

Born in Nigeria, Ikuomola said he was motivated to pursue vascular biology research by the death of his father from hypertension-induced hemorrhagic stroke as well as the deaths of cousins from diabetic coma.

Both hypertension and diabetes mellitus have been linked to the same molecular endothelial permeability mechanism that leads to sepsis.