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Search Marsden awards 2008–2017

Search awarded Marsden Fund grants 2008–2017

Fund Type: Marsden Fund

Category: Standard

Year Awarded: 2009

Title: Determining the distribution of prehistoric dryland agriculture throughout the Hawaiian Islands

Recipient(s): Associate Professor TN Ladefoged | PI | The University of Auckland

Public Summary: The complex chiefdoms of prehistoric Hawai`i developed highly intensified agricultural systems for their subsistence and ritual needs. A limited number of these have been studied in detail, but the extent and distribution of the productive base of the archipelago is unknown. The proposed research will establish the prehistoric distribution of dryland agriculture throughout the Hawaiian Islands. A GIS-based predictive model will be tested and refined with archaeological and remotely sensed data. The research will result in the development of new analytical tools and a precise and accurate quantification of the dryland agricultural component that supported the socio-political transformations of Hawai`i.

Total Awarded: $468,444

Duration: 3

Host: The University of Auckland

Contact Person: Associate Professor TN Ladefoged

Panel: EHB

Project ID: 09-UOA-171


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2016

Title: Determining the potential of the corneal Transition Zone as corneal endothelial transplants

Recipient(s): Dr J Zhang | PI | The University of Auckland
Professor CNJ McGhee | AI | The University of Auckland
Associate Professor DV Patel | AI | The University of Auckland

Public Summary: Corneal endothelial cells regulate the hydration status of the cornea but have limited ability to regenerate in vivo. Excessive loss or damage results in corneal oedema, opacity, and blindness. Current treatment is corneal transplantation whereby the diseased endothelium is replaced by donor endothelium; this approach relies heavily on a limited local and global donor cornea supply. Adult stem cells for the corneal endothelium have recently been identified in the ‘Transition Zone’ (TZ) of the cornea, but their proliferative and regenerative potential is undetermined. We aim to determine the proliferative and regenerative potential of the TZ. We will determine the ability of the TZ to stimulate endothelial regeneration by proliferation and differentiation into new endothelial cells in vitro and in an in vivo corneal endothelial injury model, and determine whether the TZ has potential to promote endothelial regeneration as an alternative to endothelial keratoplasty. If successful, each donor cornea could provide grafts for several transplants and our approach has clear ethical, lineage and safety advantages over other stem cell sources. The results will form the basis of research to understand and manipulate these cells, with the goal of treating corneal endothelial diseases.

Total Awarded: $300,000

Duration: 3

Host: The University of Auckland

Contact Person: Dr J Zhang

Panel: BMS

Project ID: 16-UOA-227


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2011

Title: Determining the role of an obligate anaerobe in intestinal barrier function

Recipient(s): Dr RC Anderson | PI | AgResearch
Dr NC Roy | AI | AgResearch
Prof JM Wells | AI | University of Wageningen

Public Summary: The human intestine contains trillions of commensal microbes which are generally regarded as having positive effects on health. 99% of the 500-1000 bacterial species residing in the large bowel are obligate anaerobes that cannot survive in the presence of oxygen; however, host-microbe interaction research has focused on oxygen-tolerant bacteria due to the difficulty of culturing oxygen-requiring intestinal cells with obligate anaerobes. We have developed a novel apical anaerobic intestinal barrier model that enables the survival of both intestinal cells and obligate anaerobes, allowing the investigation of the effects of the unstudied majority of the intestinal bacteria on human biology. This research will focus on Faecalibacterium prausnitzii which is less prevalent in people with intestinal barrier dysfunction and has anti-inflammatory properties. With our apical anaerobic intestinal barrier model it will now be possible to determine the biological mechanisms used by F. prausnitzii to maintain intestinal barrier function and immune homeostasis. Appropriate intestinal barrier function is vital in preventing antigens and pathogens from entering the body and potentially causing disease, and intestinal immune homeostasis is critical in preventing inflammatory disorders. The results will give new insights into the contribution made by a specific obligate anaerobe to healthy intestinal function.

Total Awarded: $300,000

Duration: 3

Host: AgResearch

Contact Person: Dr RC Anderson

Panel: CMP

Project ID: 11-AGR-006


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2010

Title: Developing a quantitative model library to investigate endothelial cell nitric oxide signalling as an integrated network

Recipient(s): Dr MT Cooling | PI | The University of Auckland
Prof RD Kamm | AI | Massachusetts Institute of Technology

Public Summary: The responses of endothelial cells to shear stress leading to vascular maladaptation are not fully understood. Signalling studies focus on small numbers of signalling pathways, despite a growing awareness of the need to consider complete networks. Recent advances in Systems Biology, microfluidic experimentation and modular library methodologies provide a substantial opportunity to tackle larger scale signalling projects than previously attempted. In this interdisciplinary project, we will combine modelling methods I have developed, and initiate an international collaboration in microfluidic techniques to construct the first library of realistic, modular mathematical models that together examine endothelial nitric oxide signalling at the network level.
Focusing on the initial six hours post-stimulation by shear stress, we will analyse, for the first time, the network quantitatively as a collection of inter-related functional modules, gaining a more complete understanding of the intracellular development of cardiovascular disease and how such networks function. This project will establish me as an independent research in modular signalling modelling, increase New Zealand’s skill base in microfluidic experimentation, and provide mentoring for postgraduate students. In addition, we will develop a New Zealand-based framework, in the form of an extensible, publically-available library of modular models, for quantitative signalling network research worldwide.

Total Awarded: $257,391

Duration: 3

Host: The University of Auckland

Contact Person: Dr MT Cooling

Panel: EIS

Project ID: 10-UOA-005


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2011

Title: Developing complex evaluation strategies for wicked problems

Recipient(s): Dr MD Walton | PI | Massey University

Public Summary: This research seeks to apply complexity theory to the development of policy evaluation methods. Particular types of policy problems, such as reducing rates of obesity or family violence, can be considered ‘wicked’ problems. ‘Wicked’ policy problems cannot be easily defined, and are unlikely to have a single or simple solution. Effective policies for such problems may vary across geographic and demographic communities. This variation poses a challenge for evaluating policies to inform government investment. Several authors have discussed the likely benefits of complexity theory informed evaluation, but there are few practical examples of its application. The proposed research will: review current and emerging evaluation practices; interview leaders in the field of evaluation and complexity theory; develop evaluation scenarios for two policy case studies to identify possible evaluation methods; and, test these through a workshop with evaluation practitioners and users. The results will provide a guide to evaluation approaches for 'wicked' problems consistent with complexity theory. Strengths and weaknesses of approaches, potential barriers, and implications for policy and intervention design will be considered. This research will inform evaluation practice and further research regarding complexity theory and public policy.

Total Awarded: $292,208

Duration: 3

Host: Massey University

Contact Person: Dr MD Walton

Panel: SOC

Project ID: 11-MAU-093


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2014

Title: Developing inversion methods for non-stationary thinning of point processes

Recipient(s): Dr T Wang | PI | University of Otago
Dr K Kiyosugi | AI | University of Tokyo
Associate Professor J Zhuang | AI | Institute of Statistical Mathematics

Public Summary: The whole pattern of an incomplete jigsaw puzzle can be reconstructed when missing pieces are randomly dispersed. Can we restore original point patterns when missing data exist in the long-term records of point processes related to natural or social phenomena, such as earthquakes, crime and disease prevalence? The degree of completeness of these records varies dramatically. There are more missing data from early time periods compared to recent periods, and smaller events are more likely to be missing than substantial ones. Inversion reconstructs the original process, based on a record with incomplete observations. However, existing inversion methods have been limited to the cases where the probability of missing events is stationary. This project will develop analytical and numerical methods to inverse point processes with non-stationary missing probabilities, where the probability of missing an event depends on time and event size. Particularly, we will investigate two types of missing probabilities, one being a deterministic function of time and size, and the other a stochastic function also dependent on the history of the process. The methodology developed in this research will benefit the advancement of knowledge in probability theory and contribute to applications associated with missing data problems in point processes.

Total Awarded: $300,000

Duration: 3

Host: University of Otago

Contact Person: Dr T Wang

Panel: MIS

Project ID: 14-UOO-267


Fund Type: Marsden Fund

Category: Standard

Year Awarded: 2017

Title: Developmental changes in children's learning and application of 'ground rules' during interviews about past experiences

Recipient(s): Dr DA Brown | PI | Victoria University of Wellington
Dr SP Brubacher | AI | Deakin University
Professor ME Lamb | AI | University of Cambridge
Professor C Lewis | AI | Lancaster University

Public Summary: How do children develop in their ability to understand and answer questions? From a young age children learn that they should answer adults’ questions. In some interactions, children’s answers critically affect decisions adults make. When children are questioned by doctors about their symptoms, by lawyers in family court about home life, or by social workers about possible maltreatment, their responses have serious implications. It is crucial that children do not answer questions when they are confused or uncertain. To help children recognise that adults have different expectations of them in such settings, interviewers often teach them “ground rules” – to say “I don’t know”, “I don’t understand”, or “that’s not right” when needed. Despite widespread use of ground rules, we know little about how well children of different ages understand them, what impact they have on children’s behaviour, and how they should be taught. In this project, we examine how children’s understanding and use of ground rules changes with age, and test ways of teaching the rules that are informed by cognitive research. Our findings will help adults prepare children to answer questions about their experiences, and ensure we gain better information to use for decisions about children's well-being.

Total Awarded: $840,000

Duration: 3

Host: Victoria University of Wellington

Contact Person: Dr DA Brown

Panel: EHB

Project ID: 17-VUW-142


Fund Type: Marsden Fund

Category: Standard

Year Awarded: 2014

Title: Developmental reversals in children's false memories for experienced events

Recipient(s): Dr DA Brown | PI | Victoria University of Wellington
Professor ME Lamb | AI | University of Cambridge
Professor CJ Brainerd | AI | Cornell University

Public Summary: When we remember personal experiences, we reconstruct our memory, drawing upon past knowledge to do so. This makes memory prone to error. Generally there will be no consequence arising from these errors. In contexts such as the courtroom, however, memory errors can have devastating repercussions. Younger children are perceived as less reliable eyewitnesses than older children and adults. Research in false memory has challenged this assumption, showing that under certain conditions, older children and adults are more likely to make memory errors than younger children. However, the relevance of these findings for the courtroom is uncertain because they are based on 'artificial' memory tasks (eg, remembering word lists) that are very different from experiences that require children to give evidence. Our research will test hypotheses derived from laboratory settings in a real-world context. Specifically, we will examine whether false memory for typical (but not experienced) features of a familiar event increases between early and late childhood in the same way and under the same conditions as it does for word list recall. We will also examine whether children’s performance on the different memory tasks is related, and whether specific aspects of cognition affect performance on these tasks.

Total Awarded: $585,000

Duration: 3

Host: Victoria University of Wellington

Contact Person: Dr DA Brown

Panel: EHB

Project ID: 14-VUW-115


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2014

Title: Diabetic heart pathology: is it all about the glycogen?

Recipient(s): Dr KM Mellor | PI | The University of Auckland
Professor LMD Delbridge | AI | University of Melbourne

Public Summary: Diabetic patients have a 2.5-fold increased risk of heart failure. The cardiac origins of this vulnerability are poorly understood. For over 80 years it has been known that, paradoxically, glycogen accumulates in the human diabetic heart but to date, no mechanistic explanation for this dramatic pathology has been forthcoming. Genetic glycogen storage diseases have demonstrated that excess glycogen in the heart leads to cardiac dysfunction, contractile protein disturbance, and arrhythmias. Our previous studies of diabetic cardiopathology provided the first demonstration of a role for excess ‘recycling’ of cellular components and consequent cell death through a pathway called autophagy (‘self-eating’) in diabetes. Very recently we have discovered that an autophagy pathway specific for glycogen is increased in the diabetic heart. This study aims to determine whether glycogen-specific autophagy, ‘glycophagy’, underlies increased cell death and diastolic dysfunction. Gene manipulation techniques will be used to target glycogen handling in a well defined cardiac muscle cell culture system, progressing to in vivo use to define the role of glycogen mishandling in the progression of diastolic heart failure in diabetes. In characterising glycophagy as a novel component of diabetic cardiomyopathy, this project has potential to identify new targets of therapeutic value for diabetic heart failure.

Total Awarded: $300,000

Duration: 3

Host: The University of Auckland

Contact Person: Dr KM Mellor

Panel: BMS

Project ID: 14-UOA-160


Fund Type: Marsden Fund

Category: Fast-Start

Year Awarded: 2017

Title: Diagnosing the diabetic heart

Recipient(s): Dr K Tran | PI | University of Auckland
Professor EJ Crampin | AI | University of Melbourne
Associate Professor AJ Taberner | AI | The University of Auckland

Public Summary: The heart is a complex machine. It is governed by a delicate balance of many interacting cellular processes. In disease, this balance is disturbed. This is especially relevant in diabetic heart disease, where the progression to failure is associated with changes in electrical activity, a decline in energy supply and a reduced ability of the heart to pump. Given all these changes, uncovering the mechanisms that drive the diabetic heart to fail remains an open challenge.

To uncover the mechanisms that link all these elements of failure in diabetic heart disease, we propose to use an interdisciplinary approach, integrating cell and tissue level experimentation, innovative bioinstrumentation and computational modelling. We will undertake a comprehensive series of experiments to characterise the effects of diabetes during the development to heart failure. With these data, we will build a novel computational model of diabetic cell function. We will use the model to unravel the complex interactions responsible for diabetic heart failure. The model will be used to simulate potential therapeutic treatments to identify critical time points at which an intervention could improve heart function.

Total Awarded: $300,000

Duration: 3

Host: University of Auckland

Contact Person: Dr K Tran

Panel: BMS

Project ID: 17-UOA-300


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