JCSMR Public Lecture Series

30 July 2012

The 3rd in The JCSMR Director’s Health through Discovery Public Lecture Series, which was held on 30 July, featured three JCSMR early Career Researchers. Dr Rebecca Haddock, Dr Andrew Ziolkowski and Ms Charis Teh each gave a 15 minute overview of their current research.

Sympathetic hyperactivity: A major determinant of cardiovascular disease in the obese
Dr Rebecca Haddock, Blood Vessel Group, The John Curtin School of Medical Research, ANU.
Affecting 3.7 million people, cardiovascular disease is Australia’s largest health problem. The risk of developing cardiovascular disease, including hypertension, is significantly increased in individuals who are obese or overweight. Increasingly, emerging evidence suggests that obesity-related hypertension is a distinct disease type, with disturbances in sympathetic nerve activity considered to play a critical role in the onset and progression of this disease. Our work on vascular sympathetic nerves controlling blood pressure is directed to uncovering new therapeutic targets aimed at reducing excessive nerve-mediated vasoconstriction and decreasing blood pressure in the obese.
Preventing insulin-producing beta cell failure in Type 2 diabetes
Dr Andrew Ziolkowski, Cancer and Vascular Biology Group, The John Curtin School of Medical Research, ANU.
There is a progressive deterioration in the function and number of insulin-producing beta cells in the pancreas of Type 2 diabetics (T2D). Recently, my laboratory has demonstrated that this deterioration correlates with a decline in the content of the complex carbohydrate, heparan sulfate, within beta cells, heparan sulfate being a critical carbohydrate required for the survival of insulin-producing cells. We are exploring a novel therapeutic approach for preventing T2D disease progression which involves replenishing the heparan sulfate within the insulin-producing cells with heparan sulfate-like drugs.
Multi-layered armour protects our body from “friendly fire”
Dr Charis Teh, Immunogenomics Group, The John Curtin School of Medical Research, ANU.
When the body’s defence force - immune system cells – mistakenly regards its own constituents as pathogens and launches an attack upon the body’s normal tissues this “friendly fire” results in an autoimmune disease. Although these diseases collectively affect 5-10% of Australians, the reasons for these attacks are still poorly understood, and consequently no specific prevention or treatment is currently known. We discovered that inherited changes in the genetic code can results in the failure of the body’s multi-layered armour against “friendly fire”. The discovery will help future efforts to understand how multiple changes in our genetic blueprint co-operate to shape the timing of onset and type of the organs targeted in autoimmune diseases and provide new ways to target treatment.