The latest discoveries in kidney disease were described in the winning presentation at Accesscience06, a competition at University College Dublin that challenges six postgraduate research students to explain their work in simple, jargon-free English.
Stephen Nolan claimed the honours on Tuesday with a talk titled When Good Cops Go Bad. In front of a non-scientific audience of almost 300 people, he explained his research into the way the body's own immune cells contribute to the damage seen in kidney disease.
The winners of an Accesscience06 poster design competition were also announced. The overall winner out of 180 entrants was fifth-year secondary-school student Aidan Farren, from Scoil Mhuire in Buncrana.
"I enjoyed it, it was a nice challenge," Nolan said about his win. The pleasure was less in the presentation than in taking his complex research "and turning it into something interesting to a lay audience".
As ever, RTÉ presenter Pat Kenny hosted the event, now in its 11th year, and kept the six contestants in line with a bleeper that warned if they were running over time. He also handed out the prizes afterwards.
GAA pundit and broadcaster Mícheál Ó Muircheartaigh chaired the lay judging panel, which included TV3 news anchor Claire Byrne, RTÉ radio and television presenter Shane O'Donoghue and Today FM presenter and producer Jenny Kelly.
The "cops" in the title of Nolan's presentation refer to the role played in the body by white blood cells, a key element of our immune defences against disease. Unfortunately, these same cells are an important contributor to the damage seen in kidney disease, explained Nolan. His talk described his research into how the white cells cause damage to a vital kidney cell type, proximal tubular epithelial cells.
The kidney is made up of millions of tiny tubes called nephrons, which act to filter out waste and impurities, and the epithelial cells line these tubes, Nolan explained. Diabetes, high blood pressure and certain kidney diseases can initiate damage to the epithelial cells and in the process attract the attention of the white blood cells which begin to congregate in the kidney.
This triggers additional damage to the cells in end-stage kidney disease or kidney fibrosis, Nolan said. The crowding cells release proteins that build up in the spaces between the tubular cells, squeezing them together and reducing the blood flow through them.
Nolan described how he isolated healthy white blood cells from a sample and then put them into epithelial cell cultures.
"It is an ideal way of monitoring the interaction between the two cell types," he said. "An immune signalling molecule is released by the white cells and this interacts with other cells. It causes the epithelial cells to change into fibroblast-like cells.
"Fibroblasts are involved in wound healing and scarring. When they change into fibroblast cells, they change shape, they move more and can't fit into the tubular wall like they did."
The change attracts more white cells, which cause more damage, making disease progression self-sustaining, Nolan said. "It gets to the point that the disease drives itself."
Learning these details is important, he added. "The first step in finding a cure is understanding the disease." This opens up new ways of countering the disease process.