This summer, UAB graduate student Kathryn Oliver will share her cystic fibrosis research through public talks at the Homewood and Hoover libraries. Her presentations are part of the UAB Graduate School’s Discoveries in the Making program, where graduate students and postdoctoral fellows present UAB’s newest knowledge to a general audience.

But Oliver, who is part of the Genetics, Genomics and Bioinformatics Graduate Theme, faces a problem — the complexity of her work. Her recent molecular biology publication is impenetrable to a lay reader. Its title is “Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.”

Gobbledygook

To nonscientists, that translates as “Gobbledygook partially corrects gobbledygook.” Yet this research by Oliver and colleagues is important. Some of their groundbreaking findings may yield new ways to treat people with the genetic disease cystic fibrosis. (Read more about the research in this story from UAB News.)

Oliver recently shared her thoughts on how to explain her research to the general public.

Oliver starts with the fact that cells in cystic fibrosis patients have a defect that leads to, among many other things, destructive lung infections.

“Say the lung cell is a house, and the house has a door,” she begins. “A house door opens and closes to let people in and out. In the lung cell, the door opens and closes to let small molecules and water in and out, in order to keep the cells healthy.”

Two quarts of mucus

There are hairlike cilia on top of the lung cells that actively wave, Oliver explains. The waving of the cilia acts like a conveyor belt to move mucus out of the lung to be cleared in your throat, and the cilia hairs need to stay hydrated for smooth conveyor belt operation. Mucus traps bacteria and other harmful things, which is why its transport out of your lungs is so important, and the lungs produce about two quarts of mucus every day.

“But in cystic fibrosis, the door is shut or not even there,” Oliver said. “As a result, the mucus is very dehydrated and sticky because the cilia are not lubricated enough. This means the bacteria and other pathogens are not cleared, and the lungs get infected, causing terrible, long-term respiratory problems.”

Oliver then applies her door-in-a-house analogy to the most common mutation found in cystic fibrosis, the delta-F508 mutation (ΔF508).

Too fast and sloppy

“In ΔF508, the carpentry shop workers in the cell are too fast and sloppy, so the door being made is not put together correctly,” Oliver said. “The quality control guy comes by and says, ‘Wow, this is not a good door at all; get rid of it.’”

The cystic fibrosis treatment that Oliver and colleagues have discovered tells the “hasty carpenter” to slow down. This treatment is a genetic tool used to suppress the bad carpenter, and when the researchers add another FDA-approved drug that boosts the effects of the genetic tool, they get significantly better production and operation of the door in cystic fibrosis lung cells.

Oliver and colleagues tested the treatment and obtained these promising results in cells that came from the lungs of people with cystic fibrosis, specifically those carrying the ΔF508 mutation. If clinicians can learn how to apply the treatment to patients, the conveyor belt of mucus from the lungs could start to work properly, thus reducing infections and avoiding chronic lung damage.

Help from an analogy

Oliver’s description of a house with a door to explain her research is a teaching and learning tool known as an analogy. An analogy uses familiar information to explain the unfamiliar. In her description, Oliver shows how the familiar attributes of a door — it can open and shut, and this controls the entry or exit of people — correspond to the unfamiliar attributes of her research, an ion transport channel in the membrane of a lung cell.

Using her analogy, that title of “Gobbledygook partially corrects gobbledygook,” becomes simpler. Now it can say: “Slowing down a hasty, sloppy carpenter partially corrects the broken door in cystic fibrosis.”