Improving Respiratory Transition And Outcomes Of Newborn Infants
Funder
National Health and Medical Research Council
Funding Amount
$262,251.00
Summary
Effective mask ventilation is the most important intervention at birth that can reduce mortality and disability in term and preterm infants. I will develop strategies to help clinicians improve their resuscitation skills. I will also study new ways to better support babies’ transition after birth, to improve their short and long term outcomes. The results of this research will change the way newly born babies are cared for around the world.
I am an orthopaedic surgeon and clinician-scientist based at Sydney’s largest children’s hospital. My goal is to improve treatments for children with traumatic injuries and bone deformity. I have worked in bone research for over 20 years. My current research interests are finding new treatments for drug-resistant bacterial infections, treating genetic bone disease, and developing new medical devices to help children’s bones grow straight.
A Subphenotyping Approach To Identifying Genes Responsible For Isolated Clefts Of The Lip And Palate.
Funder
National Health and Medical Research Council
Funding Amount
$679,707.00
Summary
Clefts of the lip and palate are the most common birth defects involving the face. The genes responsible for these conditions have been difficult to find in the past. We have identified a method through which the chances of finding these genes is greatly increased. Detailed measurements of a number of facial features in cleft patients and unaffected first-degree relatives will provide a much clearer picture of those at higher risk of being affected by this debilitating disorder.
Skeletal disease is a major problem for children with mucopolysaccharidoses (MPS). Patients suffer from early onset osteoporosis and osteoarthritis, severely affecting their quality of life. We will evaluate a lentiviral gene therapy vector developed in-house for its capacity to transduce bone, cartilage, synovial and ligament cells in a mouse model of MPS VI. Our goal is to generate high level, sustained expression of the deficient MPS enzyme and alter the course of skeletal disease in MPS.