 Good evening ladies and gentlemen. It's a great honor to be here, and I'm really humble especially after hearing the ratio of applicants and awardees. I would like to begin by thanking the Brain Foundation, its sponsors, donors, the scientific committee members, staff for the bestowal of this research gift. This will allow our group that sits within the Institute for Physical Activity and Nutrition at Deakin University to conduct research on this exciting new project. I also speak on behalf of my co-investigators, Professor Aaron Russell, Dr. Victoria Folletta, Dr. Paul Delegata, and Dr. Frederico Girlinger Romero. We are all very enthusiastic about the exciting possibilities of this project and very grateful for this award to help us undertake it. Sorry, this award will help us undertake this project. An aspect of our group's research is to focus and better understand how skeletal muscle maintains its strength and function. In particular, we have become interested in understanding the relationship between motor neurons and muscle and how it affects muscle health. When trauma or disease damages the connection between the motor nerve and skeletal muscle, muscle wasting occurs. This leads to impaired mobility, lack of independence, and may even lead to premature death for some people. Most peripheral nerves are able to repair and recover functional connections with the skeletal muscle. However, the amount of nerve regeneration is often not sufficient. This leads to permanent muscle weakness and long-term disability. Therefore, a major goal for treatment of nerve damage is to repair the nerve processes effectively and to facilitate maximum reconnection with muscle to allow full functional recovery. In patients with motor neuron disease, or MND, and mouse models of MND, we have observed that progressive loss of motor neuron and muscle wasting is associated with an increase in a small gene called microRNA-23a in the muscle. When we suppress microRNA-23a in a mouse model of motor neuron disease, we have observed significant improvement. Now, we want to see what happens in an acute injury, in an acute pathological condition. So we propose to investigate the effect of microRNA-23a inhibition on nerve repair using an acute nerve crush injury model. Our study will investigate how skeletal muscle strength and movement improves following nerve crush injury in mice with either normal or suppressed level of microRNA-23a. We hope this study will further inform us on the specific role microRNA-23a plays in molecular pathways during regeneration. Our work is still at its very early stages. Thank you for understanding that our idea has potential and supporting our work. I hope we'll be able to present some interesting outcomes from this research in the future. Thank you again for this gift. We really appreciate it.