Research Fund Awardees
2008
- RACP/OA fellowship
- ANZ/Wicking Trust
- Myer Foundation scholarship
- TrustCo scholarship
- ANZBMS / Macquarie Group Foundation / Osteoporosis Australia scholarship
- Sanofi Aventis/P&G Pharmaceuticals scholarship
RACP/OA fellowship
Dr Kathy Wu, ANZAC Institute, Concord Hospital
Role of androgens in bone microarchitecture in men

Dr Kathy Wu,
scholarship recipient
ANZ Wicking Trust
Dr Robin Daly, University of Melbourne, Western Hospital
'Osteo-cise' - Better Bones for Life
Dr Rob Daly,
scholarship recipient
A community, evidence-based, exercise, falls prevention and education program titled 'Osteo-cise: Better Bones for Life'. A collaborative project involving 3 centres (University of Melbourne, Western Hospital / Deakin University / Geelong Hospital) and Osteoporosis Victoria.
Myer Foundation, National Scholarship
Dr Belal Khan, University of Melbourne, Western Hospital
Dr Belal Khan,
scholarship recipient
TrustCo Scholarship
Dr Rosie Meng, Curtin University Perth
Dr Rosie Meng,
scholarship recipient
ANZBMS / Macquarie Group Foundation / Osteoporosis Australia Scholarship
Charles Chen, Institute of Bone & Joint Research, Royal North Shore Hospital
Common pathways influencing osteoporosis and atherosclerosis risk
Charles Chen,
scholarship recipient
Osteoporosis is a common skeletal disorder, affecting aging populations worldwide. There is strong evidence for a major genetic contribution to variation in bone density and bone metabolism from twin studies. Twin and family studies also show genes have a major effect on body fat, blood pressure and blood vessel function. There is evidence of inverse relationship between certain cardiovascular and bone risk factors. The proposed study will use the powerful twin model to examine the relationship between cardiovascular and bone risk factors. Twins provide advantage in medical research by reducing sample size that need to be studied due to matching for age, sex and many environmental and lifestyle factors.
Twin studies of osteoporosis have been running at the Royal North Shore Hospital since 1996, in conjunction within the Australian Twin Registry, recruiting large numbers of same sexed identical and non identical twins. Bone density has been measured and blood collected. Continued contact has been maintained with most twins by newsletters and repeat visits in many twin pairs. Given the relatively long period since baseline measurements were made, these twin studies offer the opportunity to unravel the interaction between bone, fat, cardiovascular risk factors and osteoporotic risk factors with a very large sample size and long duration of follow up (9 years).
The proposed research will investigate the following hypotheses using the powerful twin model:
- Bone mineral density (BMD) and bone strength measures are lower at clinically relevant sites in subjects who are hyperlipidemic and in subjects with impaired arterial stiffness or aortic calcification
- Loss of BMD is greater in patients with atherogenic risk factors than in subjects without them
- Atherogenic risk factors are associated with within-pair differences in biochemical markers of bone turnover and in circulating levels of relevant hormones and cytokines, demonstrable by cross-trait, cross-twin analysis in discordant twin pairs
The project is likely to lead to a better understanding of these diseases including the clinical importance of basic science in this area, better identification of those at high or low risk of the respective diseases and have therapeutic implications based upon risk factor modification.
Sanofi Aventis / P & G Pharmaceuticals scholarship - final year
Jonathan Gooi, St Vincent's Institute, University of Melbourne
Osteoclast mediated regulation of bone formation
Jonathan Gooi,
scholarship recipient
Update January 2008
As I enter the final year of my PhD, I have shown that communication between the osteoclast and osteoblast is necessary for the full effect of Teriparatide. When Teriparatide is co-administered with an osteoclast inhibitor there is a blunting of the full effect of Teriparatide, suggesting an osteoclast derived coupling signal that contributes to the osteoblasts ability to build new bone in the young growing rat.
Subsequently, whole genome microarray analysis has identified novel differentially expressed genes which may be potential 'coupling factor' candidates. The final year of my PhD will focus on examining candidate genes and their ability to stimulate osteoblasts to build new, stronger bones.
I would like to acknowledge the kind support of Sanofi-Aventis in funding the research scholarship. Without their support this work would not have been possible.

