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Auckland Medical Research Foundation awards over $1,200,000

Media Release
June 2019

Auckland Medical Research Foundation awards over $1,200,000 to medical researchers in the first half of 2019

The Auckland Medical Research Foundation (AMRF) has recently announced $1,224,626 in funding being awarded to medical researchers in its first two of five funding rounds in 2019.

“I continue to be humbled by the incredible research that is happening right here, right now in New Zealand,” says Sue Brewster, the Foundation’s Executive Director.

“It is only through the support of our very generous donors that we can continue to fund this world-class medical research and, even then, demand continues to outstrip the funding we have available with over $2.975 million requested in the latest project funding round.”

The successful grants include eight research projects ($1,031,311) awarded in Round Two, two Kelliher Charitable Trust Emerging Researcher Start-up Award ($60,000), the second instalment of Dr David Musson’s AMRF Senior Research Fellowship ($100,000), and 13 travel grants ($33,315). See below for full award summaries. Grants were awarded in a variety of biomedical, clinical and population health research areas including:

Vaccine delivery
Bone health
Post-surgical complications
Brain development
Cardiovascular disease

The Auckland Medical Research Foundation is the largest independent funder of medical research in New Zealand and provides contestable funding for medical research across the complete spectrum of modern medicine. Over the last 64 years we have distributed over $75 million in funding to a wide range of research activities – currently around $3-4 million annually.

Our Foundation is a charitable trust and is unique in the sector, in that every dollar donated from within the community goes directly and fully (100%) to research. Our administration costs are supported by a generous benefactor.

For further information on the current grants awarded and application forms for future grant rounds see our website at

Grants Awarded up to end June 2019


Dr Michal Kluger, Ms Monica Skarin, Dr David Rice, Prof Peter McNair
Anaesthesiology and Perioperative Medicine, Waitemata District Health Board

After a hip or knee joint replacement it is important to mobilise (get out of bed and move) early to recover faster, and reduce the risk of complications after surgery. Mobilisation can be hindered by orthostatic intolerance, described as the development of symptoms (dizziness, nausea, vomiting, blurred vision, feeling of heat, and fainting) when standing upright. Orthostatic intolerance has been reported to happen in up to 60% of patients after surgery. Reasons include an inability of the peripheral blood vessels to constrict (tighten) properly in response to standing. Midodrine is a drug that works by constricting the peripheral blood vessels, thereby improving blood pressure. This study aims to investigate if midodrine can reduce the occurrence of orthostatic intolerance after hip and knee joint replacements. One-hundred and seventy patients will be randomised to receive either midodrine or placebo in the early postoperative period. Orthostatic intolerance will be assessed on the day of surgery, and on the first day after surgery. Midodrine is effective in treating chronic orthostatic intolerance and we believe the administration will reduce the occurrence of orthostatic intolerance in patients after hip and knee joint replacements. This may lead to faster recovery and shorter stay in hospital.

Prof Jillian Cornish, Dr Simon Young, Dr Scott Bolam, Mr Stuart Irwin
Dept. of Medicine, The University of Auckland

Infection following joint replacement surgery is a devastating complication. It leads to prolonged hospital admissions and poor outcomes for patients and is a heavy economic burden for the health care system. With an aging population and the increased demand for joint replacements, we urgently need to reduce the incidence of infection and improve its treatment. A main challenge of joint replacement infections is the formation of bacterial biofilms on implant surfaces. Once there, the biofilms make the bacteria resistant to antibiotics and the natural defences of the body. This helps the bacteria to gain a foothold in the replaced joint, causing infection that is difficult to eliminate. We have discovered that a novel protein from milk products, lactoferrin, has a natural ability to disrupt bacterial biofilm. This makes them much more susceptible to both antibiotics and the body’s natural defences. Our project will evaluate the effectiveness of lactoferrin for both preventing and treating joint replacement infections. This will be done both in our laboratory and in a rat joint replacement infection model. We have an experienced team of orthopaedic surgeons, microbiologists and molecular biologists who can transfer the knowledge gained in our project from the laboratory to the bedside.

THE FIIX STUDY ($152,825 - two years) 1119003
Prof Cynthia Farquhar, Dr Sarah Lensen, Dr Lynn Sadler
Dept. of Obstetrics & Gynaecology, The University of Auckland

One in six New Zealand (NZ) women experience a delay in conceiving. Thirty percent of infertile couples have unexplained infertility. Currently women with unexplained infertility in NZ must have tried to conceive for five years prior to a one year waiting list for in vitro fertilisation (IVF). Our research group has recently reported that 30% of women who have three cycles of intrauterine insemination (IUI) will have a live birth. The public funding in NZ allows women to choose four cycles of IUI or one complete cycle of IVF. This study will provide data comparing four cycles of IUI and one complete cycle of IVF allowing women to be fully informed about the best strategy. We will also be considering the impact of four cycles of IUI on the subsequent two IVF cycles including cost effectiveness. If we are able to report that four cycles of IUI followed by two cycles of IVF is less expensive than two cycles of IVF then it is likely to have a global impact as then IUI can be offered as a first line alternative to IVF. The information from this study has the potential to influence policy and funding for fertility in NZ and beyond.

COLLAGEN VI KNOCKOUT ($79,593 - 2 YEARS) 1119001
Dr David Crossman, Dr Carolyn Barrett, Prof Christian Soeller, Prof Peter Ruygrok, Pro Bruce Smaill, Dr David Baddeley, Dr Prasanna Kallingappa
Dept. of Physiology, The University of Auckland

Human heart failure is the inability of the heart to pump enough blood to meet the energetic demands of an active lifestyle. This condition results from cardiac muscle cells losing their ability to contract. This is a serious health condition and a major cause of death of New Zealanders. Through previous research support from Auckland Medical Research Foundation, we have identified collagen VI is likely responsible for damaging the electrical connections responsible for signalling muscle cell contraction. In this project, we will test if removal of collagen VI can be used to prevent damage to these electrical connections and improve cardiac function after myocardial infarction. This will be done by using our state-of-the-art super-resolution microscope to image, at the nano-scale, the structure of these critical electrical connections.

Dr Rashika Karunasinghe, Dr Justin Dean, Prof Janusz Lipski
Dept. of Physiology, The University of Auckland

Our ability to form memories and learn is fundamental to the way we experience life. These processes are coordinated by highly-specific and wire-like connections from neuronal cells in the hippocampal region of the brain, which mostly develop before birth and during early childhood. However, these become disrupted in infants diagnosed with brain injury after low oxygen and glucose availability during birth. Survivors show abnormal neuron growth and activity (typified by seizures and learning problems), affecting brain functions throughout later life. However, scientists and clinicians are still challenged by why and how low oxygen and glucose affects neuronal development. We recently found that young neurons produce a key sugar called ‘hyaluronan’, which normally controls their growth. However, experimentally restricting brain blood flow, and thereby limiting oxygen and glucose supply, caused a loss of brain hyaluronan. We now propose that a loss of hyaluronan causes the abnormal neuronal development in young infants. The main objective of this study is to explore how abnormal levels of hyaluronan may alter hippocampal neuron development following a reduction in the supply of oxygen and glucose to the brain. The ultimate goal is to explore whether hyaluronan can restore brain development in affected infants.

A/Prof James Fisher, Prof Julian Paton
Dept. of Physiology, The University of Auckland

One in three New Zealanders have high blood pressure, which can cause stroke, kidney and heart failure. Its asymptomatic characteristic means it can go undetected. More alarming is that half of those patients on medication do not have their blood pressure controlled suggesting that current medications are not effective. The proposed project will establish if the reason blood pressure goes up relates to changes in the detectors of carbon dioxide (CO2), a product of metabolism, in blood. These detectors are located in the carotid arteries and the brainstem and powerfully increase blood pressure when stimulated. Patients will be recruited from a recently formed high blood pressure network spanning five district health boards. In a brand new specialist Human Research Laboratory within the ADHB, we will determine whether CO2 detectors are sensitised in people with high blood pressure. We believe they are and that the detectors in the carotid artery are, in part, responsible for the sensitivity of brainstem CO2 detectors. Our findings may reveal a novel mechanism for why people become hypertensive. This information will be critical for developing new management strategies to control blood pressure using both repurposed drugs and medical devices, which may become available to us in due course.

Dr Catherine Crofts, Mrs Marie Mckay, Dr Amira Hassouna
School of Interprofessional Health Studies, Auckland University of Technology

People with high blood insulin levels have a high risk of developing type 2 diabetes, heart disease, certain cancers or dementia. We want to find a simple test for identifying these people and monitoring whether lifestyle changes can keep their blood insulin levels low and decrease their risk of these diseases. We have access to the BioVolt point-of-care device that will measure insulin levels through a fingerstick blood sample. Before we can use this device, we need to first prove that it is as accurate as the normal laboratory testing processes. We are also concerned that insulin levels in capillary (fingerprick) blood may be different to that in the usual sample of venous blood. We plan to compare the insulin levels between venous and fingerstick blood samples on both the BioVolt device and though normal practices. Once tested, we want to use the BioVolt device in both research and clinical practice to help keep people healthy.

Dr Annika Winbo, A/Prof Johanna Montgomery, Prof Jonathan Skinner
Dept. of Physiology, The University of Auckland

In this study we will use our combined expertise in clinical cardiology, cardiac electrophysiology and neurophysiology to perform novel research into the interactions between sympathetic neurons and heart cells in inherited arrhythmia syndromes. Specifically, we will focus on Long QT Syndrome (LQTS), the most common cause of sudden death in New Zealand youth. LQTS arrhythmias are typically triggered by the sympathetic “fight-or-flight” response. Treatment strategies including beta-blockers and sympathectomy (the surgical cutting of a sympathetic nerve to break the neuron-heart cell connection), although the underlying mechanisms remain poorly understood. Also, exactly how these sympathetic neurons cause cardiac arrhythmia in LQTS is unknown. Recent breakthroughs make it possible to model neuro-cardiac interactions in vitro. Using induced pluripotent stem cells (iPS cells) that we have reprogrammed from LQTS patient and control blood, we will grow sympathetic neurons and heart cells together. These co-cultures will enable us to directly study the neuronal regulation of heart rate and action potential duration using cellular electrophysiology techniques, and find out what differs in the LQTS patient-derived cells that causes the arrhythmia. A better understanding of the underlying neurocardiac arrhythmia mechanisms could enable improved risk management, tailored therapies and new treatment targets for LQTS families.


$30,000 – 1719001

Dr Sarah Stewart
Department of Medicine, The University of Auckland

Research support for her Postdoctoral Fellowship ‘Ultrasound in asymptomatic hyperuricemia’

$30,000 – 1719002

Dr Jia-Yun Tsai
Department of Molecular Medicine & Pathology, The University of Auckland

Research support for her Postdoctoral Fellowship ‘A novel peptide delivery platform for the development of mucosal vaccines’


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