Awarded Fellowships and Scholarships

Fellowship and Doctoral Scholarships awarded 2013

  • 01 Jan 2014



Dr Andrew Wood
Dept of Molecular Medicine and Pathology, University of Auckland

Acute Myeloid Leukaemia (AML) is a blood cancer that is frequently fatal despite intensive chemotherapy and stem cell transplantation. Spelling mistakes accumulate in the DNA instructions that control how a cell behaves with the result that white blood cells keep reproducing until they overtake the body leading to clinical symptoms. By sequencing leukaemias from many people we have built up catalogues that list the various spelling mistakes, but it is not always clear how to translate this knowledge into better treatments. In children with AML the gene ETV6 is frequently mutated, and although a lot is known about this gene in health and other cancers very little is understood about why it makes AML in children so hard to cure. In this research we aim to find out how ETV6 mutations work by introducing them into zebrafish. We hope the mutations will change the way leukaemias grows in fish, and that by studying this we will learn the leukaemia’s weak spot. Then we will use robots to treat thousands of zebrafish with thousands of drugs to see if any kill ETV6 leukaemia. If successful this study will identify compounds that can use to better treat ETV6 driven leukaemias in patients.



MANAGEMENT OF NEONATAL HYPERGLYCAEMIA  – 1413002 ($257,333 – 3 years)

Dr Kathryn Williamson
Newborn Services, Auckland City Hospital

Babies who are born very preterm have a high risk of suffering brain damage. High blood sugar levels (hyperglycaemia) are common in these very small babies, and are associated with poor outcome. Hyperglycaemia is usually treated with insulin, but in very small babies the correct dose of insulin can be difficult to determine and babies’ insulin requirements can fluctuate over a short period of time. This means that sometimes the babies’ blood sugar level can fall too low (hypoglycaemia). Unfortunately, hypoglycaemia can put babies at further risk of brain damage. A computer program has been developed to help keep blood sugar levels in a safe range for preterm babies treated with insulin. We will determine if this computer program can reduce the incidence of hypoglycaemia, and also whether it improves growth and later development. If effective, this computer program will be incorporated into routine care of preterm babies in New Zealand and worldwide, potentially reducing the burden of brain damage after preterm birth.

Guardian Trust

Funded by: Ruth Spencer Trust


Postdoctoral Fellowships



Dr Natasha Grimsey
Centre for Brain Research, University of Auckland

Mental illnesses such as depression, bipolar disorder and schizophrenia affect around16% of New Zealanders. Most of these conditions are difficult to diagnose and treat effectively. Continued research is required to better understand these disorders and develop new medicines. The mind-altering properties of cannabis have been recognised for centuries, but the proteins in the brain that allow cannabis to exert its effects have only been identified in the last two decades. These proteins are called Cannabinoid Receptors 1 and 2, and as well as responding to cannabis these control many normal bodily functions. All the proteins in our bodies are produced from DNA blueprints. Slight differences in these instructions between individuals can result in subtly different versions of the same protein which might work differently. A few specific versions of Cannabinoid Receptor 2 are more common in patients suffering from mental illness than in the general population. This may indicate that these versions play a role in these diseases. In this research I plan to investigate what is different about the function of these versions of the Cannabinoid Receptor. This information will provide new insight into the causes of mental illness and may assist with designing new therapies.

Guardian Trust

Funded by: Edith C Coan Trust




Dr Clare Reynolds
Liggins Institute, University of Auckland

Unbalanced maternal nutrition, whether it be over-nutrition or under-nutrition, predisposes or “programs” offspring to obesity, type-2 diabetes and cardiovascular disease in later life. These conditions are associated with chronic low-grade inflammation, however little is known in regards to the impact of maternal diet-induced programming of the offspring immune system and its subsequent impact on metabolic function and indeed chronic disease later in life. We aim to investigate obesity-induced inflammation during pregnancy and subsequent long-term offspring disease in an established rat model of maternal diet-induced obesity. We will assess the origins of inflammation in mothers and offspring by characterizing inflammation in the placenta, bone marrow and cells of the immune system. Furthermore we will determine the effectiveness of the anti-inflammatory lipid c9, t11 conjugated linoleic acid (CLA) as a therapeutic option for the reversal of maternal over-nutrition induced developmental programming. This project will allow us to establish the importance of immune mediators in developmental programming of obesity and metabolic complications and potentially develop a viable anti-inflammatory nutrient based therapeutic strategy for combatting the origins of metabolic disease.

Guardian Trust

Funded by: David and Cassie Anderson Medical Trust


Doctoral Fellowships


MATERNAL THERAPY AND THE FETUS – 1213003 ($126,000 – 3 years)

Mr Christopher Lear
Dept of Physiology, University of Auckland

Brain injury after preterm birth now contributes more than a third of all cases of cerebral palsy. We now know that even babies born prematurely without brain injury have a high risk of long-term disability and learning difficulties. Mothers who are about to deliver prematurely are almost universally given treatments such as steroids and magnesium sulphate to reduce the risk of death and many newborn complications after preterm birth. Given how often our youngest and most vulnerable infants are exposed to these treatments, it is vital to understand their effects on the preterm brain. We have recently shown that a clinical course of maternal steroids triggers transient abnormal brain activity in preterm animals, and can worsen injury during exposure to low oxygen levels. The long-term effects are unknown. In this study, I will examine the long-term impact of exposure to maternal steroids on brain activity and structure, how timing of treatment affects the response to low oxygen, and finally, whether magnesium sulphate treatment can alleviate the adverse effects of steroids on the brain. This will be providing critical new information to help guide the clinical treatment of women at risk of preterm delivery.

Guardian Trust

Funded by: Barbara Basham Medical Charitable Trust


MOLECULAR IMAGING OF LENS CATARACT – 1213004 ($126,000 – 3 years)

Mr Mitchell Nye-Wood
School of Medical Sciences, University of Auckland

Cataract is primarily a disease of old age and Age-Related Nuclear (ARN) cataract is the leading cause of blindness in the world today. ARN cataract is characterised by irreversible protein modifications in the centre or nucleus of the lens. Antioxidants in the young lens usually provide protection against this oxidative damage but an age-dependent decline in antioxidants, specifically in the lens nucleus, allows damaged protein to accumulate, eventually leading to protein precipitation, loss of transparency and cataract formation. In this study we investigate the mechanistic link between the antioxidant decline in the lens nucleus, oxidative damage to lens proteins and the loss of lens transparency using an animal model of ARN cataract. To achieve this, changes in the distribution of antioxidants and oxidative damage to lens proteins will be spatially mapped using imaging mass spectrometry, a technique that can identify and localise small molecules and large proteins in tissue sections. The effect of these biochemical changes on lens transparency will then be determined by measuring the optical properties of lens. Our study of how antioxidant depletion specifically in the lens nucleus affects overall lens transparency, will aid our efforts to develop medical therapies to delay the onset of ARN cataract.


MESENCHYMAL STEM CELLS AND IUGAR – 1213001 ($126,000 – 3 years)

Miss Megan Alexander
Dept of Obstetrics & Gynaecology, University of Auckland

A healthy placenta is the cornerstone to a successful pregnancy and delivery of a healthy baby. Insufficient placental development can lead to life-threatening pregnancy disorders such as pre-eclampsia (hypertension in pregnancy) and intrauterine growth restriction (IUGR, small babies), which have lifelong consequences. We currently know surprisingly little about the pathophysiology of pregnancy disorders, and have no effective treatments to remedy these conditions. Recent trials in other organ systems have highlighted the therapeutic potential of mesenchymal stem cells (MSC) for a range of applications. In the placenta, MSC are present throughout gestation and may contribute to creating an adequate vascular network, which is key for foetal growth. Therefore, MSC provide a promising target to improve placental vascularisation in IUGR pregnancies. This project aims to explore this potential by determining how MSC may contribute to the pathophysiology of IUGR, and whether transplantation of MSC into placentae can stimulate placental angiogenesis via direct engraftment into the placental vasculature or by paracrine mechanisms. This proof of principle work will allow the future development of MSC as a therapy for failing placentae, helping improve the lives of around 5000 babies and their mothers affected by IUGR each year.



THE SYNAPTIC BASIS OF HUNTINGTON’S DISEASE – 1213002 ($126,000 – 3 years)

Mr Wojciech Ambroziak
Dept of Physiology & Centre for Brain Research, University of Auckland

Currently one in five New Zealanders are affected by neurological diseases and as the population ages this number will considerably increase. All neurological diseases have direct or indirect effects on synapses in the brain. This project is to determine the source of synapse dysfunction in Huntington’s Disease (HD). HD is one of the most debilitating, incurable adult onset diseases with very dramatic course. Studies on HD mouse models have shown that an increase in NMDA receptors located outside of the synapse causes early synapse dysfunction that may underlie the cognitive and motor deficits seen in HD. A protein called SAP97 plays distinct roles in regulating receptor distribution within synapses, with aSAP97 regulating synaptic receptors versus bSAP97 regulating receptors outside of the synapse. Recent data suggest that this protein is a causative agent in the early pathogenesis of HD. The aims of this PhD project are to determine the role of each SAP97 isoform in the changes in NMDA receptor localisation in a cellular model of HD and if SAP97 isoform expression levels can be specifically targeted to rescue normal receptor distribution and synapse function in animal model, thus whether SAP97 isoforms are a potential therapeutic target.

Guardian Trust

Funded by: Henry Cotton Charitable Trust

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