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Tissue from hospital operating theatre to be rushed to UC

Published: Thu 28 Aug 2014 09:20 AM
Tissue from hospital operating theatre to be rushed to UC for research
August 28, 2014
Tissues blocking arteries to the brain are to be rushed to the University of Canterbury from Christchurch Hospital operating theatre to be kept alive in a laboratory for five days as part of a New Zealand Heart Foundation funded three-year study into heart and vascular disease.
The university’s medical biochemist, Associate Professor Steve Gieseg, in collaboration with Professor Justin Roake of Christchurch Hospital’s Department of Surgery, will research how white blood cells full of cholesterol in the walls of arteries causes heart disease and strokes.
Artery disease is the leading cause of deaths in New Zealand, accounting for 30 percent of deaths annually. Every 90 minutes a New Zealander dies from coronary heart disease.
The collection of the cells form growths in the artery wall which sometimes have to be removed by surgery as they are blocking the supply of blood to the organs.
``This research is important because we are examining actual plaque and human cells so we can identify key changes in the plaque and blood chemistry so allowing better identification of at risk patients,’’ Associate Professor Gieseg says.
``Tissue taken during surgery will be rushed to the laboratory at the University of Canterbury within 60 minutes of removal. The tissue will be keep alive and functioning for up to five days in the cell culture laboratory in the School of Biological Sciences.
``We will test basic ideas on how the cells respond to cholesterol particles in real patient tissue. We will compare the results to that seen with white blood cells purified from human blood.
``White bloods cells are relatively tough as they have to survive in the hostile environment of infected tissue. Yet when white blood cells encounter damaged cholesterol particles in the wall of arties they often die.
``It is the collection of these dead and dying white blood cells which forms the growths called plaques within the artery wall. The plaques can grow to the point they block the flow of blood. By examining live samples of tissue actually causing artery blockages this research will identify some of the key mechanisms of the cell death. It will also show how the changes in blood chemistry observed in these patients is linked to white blood cells’ reactions in the artery wall.’’
ends

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