NZ Summer Scholarships

Applications for the 2017/18 New Zealand Heart Research Summer Scholarship Program have now closed.

Thank you for your interest. We encourage you to regularly check back to see what other opportunities you may be eligible to apply for in the future.

New Zealand Heart Research Summer Scholarship Program

The Heart Research Institute is excited to offer a number of Summer Undergraduate Scholarships to New Zealand's best and brightest young researchers. 

These scholarships provide high-achieving and promising Kiwi students the opportunity to work on a medical research project directly related to cardiovascular disease, expand on their skills and knowledge, and be mentored in a world-class research institute. Scholarship recipients are expected to write a report on their work experience and will have the opportunity to make a presentation to their peers and supervisors at the end of the scholarship period.

These summer scholarships will take place in Sydney, Australia over the Australian summer holidays for eight weeks. Placements are full-time and typically begin early December 2017 to January 2018. 

Check out our 2016 NZ Scholarship winners and learn about their experiences.

Projects on Offer

Please read through the scientific projects on offer below. You will be asked to place the projects in order of preference in the application process. 

Post-doctorate scientists will provide mentorship, leadership and provide regular feedback, with Group Leaders overseeing.

Facilities

All projects will be carried out at our laboratories in Newtown (Sydney, Australia) or the Charles Perkins Centre at the University of Sydney

Explore our Newtown facilities in this virtual tour.

Selection Criteria

Applications will be assessed by senior HRI scientists on the basis of academic merit and suitability. Applications must include: 

  • a one-page cover letter outlining your reasons for applying and your interests in research

  • your academic record (including certified academic transcript for current degree)

  • your CV including referees (a summary of your work experience and other relevant activities)

  • projects in order of preference

All applications must fit within one of the projects outlined below. Applicants can rank their choices in order of project preference. Please submit the application all together in one PDF document. 

Applications must be received no later than 20th August 2017.

Stipend

Successful students will receive a total stipend of approximately NZ$5,400. Payment will be made in monthly instalments. 

Return flights to Sydney and accommodation at a nearby College in Sydney will be organised and paid for by the HRI. This College is within walking distance of the HRI and all the buzz of Newtown.

2017/18 Scientific Projects on Offer

Identification of a new thrombosis mechanism triggered by dying platelets
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Group: Thrombosis

Group Leader: Professor Shaun Jackson

A severe reduction in blood flow (ischaemia) to the intestines can trigger blood clot formation (thrombosis) in multiple organs, including the lungs. Gut ischaemia and subsequent pulmonary thrombosis has a very poor prognosis, with a ~90% mortality rate. While this phenomenon is common in critically ill patients, and considered a fundamental issue in critical care medicine, the mechanisms by which gut ischemia promotes pulmonary thrombosis remain unknown. Moreover, there are currently no effective antithrombotic approaches available to prevent or treat this lethal condition.

We have identified a previously unrecognized blood clotting mechanism that links gut ischemia to remote lung injury. This atypical thrombosis mechanism is triggered by dying platelets in the ischemic gut microcirculation; where dying platelets are fragmented by leukocytes and act as a bridge between adjacent leukocytes, leading to the assembly of large leukocyte aggregates that obstruct both major pulmonary vessels and the microcirculation in arteries and veins. The clinical relevance of such leukocyte-mediated thrombosis is highlighted by the presence of leukocyte-rich thrombi in the pulmonary vasculature of patients with Acute Respiratory Distress Syndrome - a serious medical condition where gut ischemia and pulmonary thrombosis are associated with a high mortality. In this project, we aim to elucidate the mechanisms by which dying platelets and leukocytes cooperatively trigger thrombosis locally in the ischemic gut and remotely in the lung. This proposal will also investigate whether targeting platelet death pathways can reduce atypical leukocyte-mediated thrombosis; with the end goal of prevent lethal pulmonary thrombosis in critically ill patients.

Investigating the link between oxidative stress and biomechanical integrin activation in diabetes
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Group: Thrombosis

Group Leader: Professor Shaun Jackson

Diabetes represents a serious healthcare problem globally. Up to 70% of all diabetes-related deaths are due to cardiovascular disease, primarily attributed to the development of blood clots in the circulation of the heart and brain (heart attack/stroke). The blood clotting mechanism is ‘hyperactive’ in diabetes, although the reason for this is not well defined. Diabetes enhances the atherosclerotic process in large arteries, increasing the risk of acute myocardial infarction (heart attack), cerebral infarction (ischemic stroke) and peripheral vascular disease. In addition to developing more extensive atherosclerosis, diabetic individuals also exhibit an enhanced blood clotting tendency (prothrombotic phenotype) that manifests as an exaggerated accumulation of platelets at sites of plaque disruption. However, the mechanisms by which diabetes causes platelet hyperactivity and enhanced blood clotting remain incompletely understood. We have recently defined a new mechanism promoting arterial thrombus formation that involves biomechanical (rheology-dependent) platelet activation, leading to the aggregation of discoid platelets. Importantly, this biomechanical platelet activation is not inhibited by conventional antiplatelet agents such as aspirin and clopidogrel, which demonstrate reduced antithrombotic efficacy in individuals with diabetes. In this project, we will compare healthy and diabetic human or mouse platelets, to examine whether this aggregation mechanism is dysregulated in diabetes. We will also examine the role chronic oxidative stress plays in amplifying blood clotting in diabetes, and the mechanisms by which oxidative stress may modify platelet receptors to enhance adhesion. These studies may identify novel targets with which to to treat thrombosis associated with diabetes.

 

Investigating the composition of occlusive arterial blood clots – development of high resolution con
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Group: Thrombosis

Group Leader: Professor Shaun Jackson

Our laboratory is currently using tissue clearing techniques to push the conventional boundaries associated with confocal microscopy by imaging deeper into tissues. Clearing methods are used to "equalize" the refractive index without destroying the three-dimensional structure and without degradation of possible fluorochromes present in the tissue. Scientists in our lab have developed a novel mouse model of carotid artery occlusion whereby clots form as a result of an electrolytic injury. Carotid tissue that has undergone injury using this model (as well as potential brain tissue from stroke models) will be collected, cleared and imaged to determine the structural make up of clots that have formed as a result of vascular injury as well as clots that may form in the cerebral vasculature. To achieve this we will clear tissues using the clearing agent BABB (Benzyl Alcohol-Benzoate Benzoate). 

During this project, you will (i) learn about advanced confocal microscopy, (ii) review the literature to understand how tissue clearing can enable us to view deeper into tissues as well as components of clot structure, and (iii) learn about tissue clearing first-hand, by preparing samples, imaging tissue and working alongside scientists currently using these techniques to establish the composition of clots formed in mouse carotid arteries as well as in the mouse brain vasculature.

Protecting against metabolic depletion to preserve the function of stored platelets for transfusion
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Group: Thrombosis Group

Group Leader: Professor Shaun Jackson

Blood products including platelet concentrates are used in hospitals across Australia every day in an effort to control/prevent bleeding and save lives. The collection, processing and distribution of these blood products is facilitated by voluntary blood donations, at an annual cost to the Australian government of over $1.1 billion. Despite their life-saving utility, when compared to other standard commercial pharmaceutical therapies, pooled platelet concentrates are relatively poorly characterised with widely varying therapeutic efficacy over their shelf-life. This stems from a well described phenomenon known as the known as the Platelet Storage Lesion (PSL), wherein the shelf-life for stored platelet concentrates is currently limited to 5 days, in order to limit bacterial contamination and the effects of PSL on platelet function. Despite decades of research characterising PSL, it remains the predominant limiting factor in the shelf-life of stored platelets, resulting in ~13% of issued platelet units and over $3.5 million lost to wastage in the 2013/4 financial year alone.

Previous attempts to limit the deterioration of platelet stored ex vivo have yielded limited success, highlighting the need for a greater understanding of the early events precipitating PSL. In studies leading up to this proposal, we have identified an unexpected and specific role for the signalling adaptor protein 14-3-3z, in the modulation of platelet bioenergetics, resulting in reduced ATP depletion and PS exposure during platelet activation. Our studies have traced the role of 14-3-3z to the mitochondria, where it appears to regulate mitochondrial respiratory reserve, enabling platelets to more readily “cope” under conditions of metabolic stress (Schoenwaelder et al, Nature Communications, 2016). In this proposal, we will explore the intriguing possibility that pharmacological manipulation of 14-3-3z can preserve platelet energy stores and reduce the impact of the PSL, facilitating a more efficient use of this precious biological commodity.

 

Novel regulators of platelet procoagulant activity – Targeting safer anticoagulation
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Group: Thrombosis Group

Group Leader: Professor Shaun Jackson

Antithrombotic therapies, which primarily consist of anti-platelet and anticoagulant agents, have become the cornerstone therapies for a wide variety of cardiovascular diseases. All currently employed anticoagulant agents indiscriminately inhibit coagulation reactions at the injured vessel wall and throughout the body of a developing blood clot, thereby increasing the bleeding risk for patients receiving these medications. The blood clotting process is driven by coagulation factors present in the plasma. These factors assemble on negatively charged surfaces, such as phosphatidylserine (PS), to facilitate thrombin generation and promote blood clot formation. Platelets also expose PS on their surface following potent activation, a process that further promotes coagulation and is referred to as platelet ‘procoagulant’ function. Recent progress in understanding the mechanisms by which platelets can support blood coagulation have raised the possibility that selective inhibition of “platelet-specific” procoagulant pathways may specifically reduce thrombin generation within a blood clot, potenitally providing a novel and safer approach to reducing blood clotting However, the exact pathways that regulate platelet procoagulant function requires further investigation.

Our laboratory has recently defined an important role for the necrotic cell death pathway in partially regulating platelet procoagulant function. In addition, we have also identified a distinct process regulating the platelet procoagulant response that involves the signalling adaptor protein 14-3-3z. We have found that 14-3-3z plays an important role in regulating platelet phosphatidylserine (PS) exposure and thrombin generation, necessary for blood clot growth and stability. We aim to determine whether therapeutic targeting of this pathway, either alone, or in combination with necrotic cell death pathways, represents a safe and effective way of reducing thrombin generation in vivo without increasing bleeding risk.

 

New approaches to the treatment of ischaemic stroke
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Group: Thrombosis Group

Group Leader: Professor Shaun Jackson

The development of a blood clot in the cerebral circulation (ischaemic stroke) is the third most common cause of death and the most common cause of adult disability globally. The central goal of stroke therapy is the prompt reperfusion of occluded blood vessels to minimise tissue death. The delivery of fibrinolytic agents modelled on tissue-type plasminogen activator (t-PA) is the only clinically approved means available to stroke patients. Despite this, the use of t-PA is associated with significant side-effects, limiting its widespread use. We are working on a novel approach to improve upon existing stroke therapies, making them safer and more effective. This novel approach utilises a new class of anticlotting medicines targeting the enzyme ‘PI 3-kinase’ (PI3K), which we first described in 2005. PI3K inhibitors have recently been trialled in humans and have been shown to be safe and effective anticlotting agents, and we now have evidence that they can safely improve t-PA-mediated blood clot dissolution. Ongoing studies using a novel mouse model of thrombolysis (iCAT) developed in our lab will determine whether cerebral damage and cognitive impairment associated with stroke are reduced using this approach.

 

Tissue Engineering New Biomaterials for Treating Cardiovascular Disease
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Group: Applied Materials Group

Group Leader: Dr Steven Wise

A major interest of our group involves the development of new synthetic materials that can be effectively used for treatment of cardiovascular disease. Despite the increasing incidence of heart disease, there are few effective biomaterials currently available for clinical vascular applications, including vascular conduits for bypass grafting and endografts for minimally invasive bypass procedures. An established treatment for clinical manifestations of atherosclerosis is the insertion of bypass grafts around an occluded arterial segment. The most common vascular grafts used are saphenous vein or mammary artery from the patient. However, although the mammary artery provides a potentially durable conduit, it may not always be the proper size or length. Saphenous vein grafts are susceptible to accelerated atherosclerosis such that by 10 years after coronary bypass grafting, 70% of vein grafts are either occluded or critically stenosed. Furthermore, the supply of artery or vein may not be sufficient or suitable for multiple bypass or repeat procedures, necessitating the use of other materials.

Currently, the principal synthetic graft materials used are woven polyethylene tetraphtlate (Dacron) and expanded polytetrafluoroethylene (ePTFE). These graft materials are rigid compared to the host artery, thrombogenic and do not readily facilitate endothelialisation. While Dacron and ePTFE perform satisfactorily as large diameter high-flow grafts (e.g. aortic-iliac replacement grafts), their use as small diameter (<6mm) vascular conduits (e.g. coronary artery or peripheral bypass surgery) has been associated with extremely high failure rates, such that no synthetic grafts are currently effective for coronary grafting, the most common bypass procedure. By using new tissue engineering methods, including electrospinning and plasma treatment, our group seeks to develop synthetic bypass grafts that closely mimic the properties of the human artery.  We use histopathology and immunohistochemistry to quantify the responses to our new materials. An effective synthetic vascular graft would revolutionise the treatment of cardiovascular disease, meeting a significant and critical unmet need.

Computational Fluid Dynamics of the Thoracic Aorta
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Group: Cardiac Imaging

Group Leader: Professor Stuart Grieve

The goal of this project is to use computational fluid dynamics (CFD) to model the contribution of abnormal aortic haemodynamics to thoracic aortic aneurysm (TAA) progression. Our laboratory has developed a capacity to accurately derive wall shear stress (WSS) and to simulated abnormal flow patterns using CT angiographic data. The project will apply these tools to a carefully selected cohort of patients drawn from the aortic dilatation clinic at Royal Prince Alfred Hospital.

Background: The impact of thoracic aortic aneurysm disease (TAA) is often underestimated. Approximately 1 in 500 people have TAA and many will die of a related complication. Rupture and dissection of TAA results in 47,0000 deaths in the USA and over 3,000 deaths in Australia per year2. Aortic diameter alone is a very poor predictor of outcome and complications but is universally used to guide treatment – despite more than 50% of complications occurring at a diameter less than the currently recommended operative cut-point3. This project will evaluate the contribution of abnormal aortic haemodynamics to diameter progression in TAA.

Project description and timeline: The project will provide the successful applicant with a solid introduction to CFD and medical imaging, and would be expected to result in a paper. The methodology has already been established, and a retrospective cohort of patients organised into three categories based on rate of aneurysm progression (stable, slow, fast progression) has been collected. The analysis will involved applying and understanding our existing techniques to this dataset, then close under supervision, interpreting and analysing the data to produce a manuscript.