Dr Natalie Pecheniuk

Biography

I am a Senior Lecturer in School of Biomedical Sciences, Faculty of Health, at Queensland University of Technology (QUT). In this position, I am significantly involved in teaching foundational biomedical science skills, biochemistry and quantitative skills. I am well versed in teaching extremely large cohorts of multidisciplinary cohorts including Biomedical Science, Medical Laboratory Science, Pharmacy and Nutrition & Dietetics students.

I received my PhD on The Genetic Basis of Thrombophilia. Then completed post-doctoral studies moving into a Staff Scientist position at The Scripps Research Institute in La Jolla, California, USA focusing on the biochemistry/molecular biology of the Protein C pathway and role of lipids and lipoproteins (HDL) as cofactors in this pathway. Upon return to Australia, I had an academic/lecturing role at James Cook University, Townsville, QLD where I also had a role as academic advisor for biochemistry/molecular biology.  In 2010 I was awarded the Kanematsu Memorial Award for work on anticoagulant activity of HDL. I have also supervised numerous Honours and research students, and currently supervising 3 PhD students. My research interests have spanned a variety of areas of thrombosis and haemostasis from the genetic basis of thrombophilia, the cofactor activity of lipid/lipoproteins on the Protein C pathway and currently is focused on coagulopathy associated with transfusion, where I have strong collaborations and hold a Visiting Research Fellowship with Australian Red Cross Lifeblood.

Research:  Blood clots are the leading cause of death in Australia and are associated with stroke, deep vein thrombosis (DVT), pulmonary embolism (PE) and coronary heart disease. Approximately 30,000 Australians are hospitalised each year due to DVT and/or PE. Haemostasis is the biological process that occurs in response to vascular trauma to prevent blood loss from the body. The blood coagulation pathway results from a cascade of protease (protein) activations to form thrombin, a key player in the formation of the fibrin blood clot. Blood clotting is also controlled by anticoagulant pathways and clots dissolved by fibrinolysis in order to prevent deleterious thrombosis from occurring. Risk factors for excessive clotting (or thrombosis) include biochemical, genetic and circumstantial events. Therefore, this is a complex process requiring balanced interaction of the endothelium, platelets and proteins involved in procoagulant, anticoagulant and fibrinolytic pathways; if the balance is tipped in favour of coagulation, thrombosis may result.

The research interests of the lab are focused on 1) the mechanisms of the biochemical or genetic risks on blood coagulation pathways 2) translational research investigating thrombotic phenotype or coagulopathy association with other clinical conditions and 3) role of transfusion and blood products with coagulation.