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NZDep2018 analysis of census 2018 variables - TA032: Central Hawke's Bay District
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/
NZDep2018 analysis of census 2018 variables - TA033: New Plymouth District
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/
Testing the connectivity of Dissostichus eleginoides (Patagonian toothfish) between the Pacific coast of southern Chile and the Patagonian Shelf in the southwest Atlantic
No full textPatagonian toothfish, Dissostichus eleginoides, are endemic to the Southern Hemisphere and are
commonly associated with sub-Antarctic Islands and seamounts. They are found around the Falkland Islands and an economically valuable long-line fishery, targeting adult toothfish, operates in the Falkland Island Conservation Zones year round. This research explores gaps in the understanding of toothfish early life history by conducting egg buoyancy experiments and particle tracking simulations to resolve important spawning locations, transport pathways and larval retention areas.
Buoyancy of toothfish eggs was estimated up to 21 days post fertilisation. Egg buoyancy followed a similar pattern to other species, where buoyancy initially decreased for several days before returning toward its initial value, although further data is needed to confirm this. Particle tracking simulations were undertaken using the software ICHTHYOP. Particles were released from potential spawning areas around the Burdwood Bank and southern Chile during July 2009 and 2012. These simulations represented spawning corresponding to a good and poor recruitment year respectively.
Results of these particle tracking simulations for 2009 and 2012 suggest that transport from the Burdwood Bank is unlikely to be a major contributor to the recruitment of juveniles around the Falkland Islands or the Patagonian Shelf, with low connectivity (50%),
indicating that larval transport from southern Chile to this area may be important for successful recruitment of juveniles around the Falkland Islands. Connectivity between these areas was weaker in 2012, potentially due to changes in the position and/or density of the boundary current that flows around southern Chile, forced by changes in the phase of the Southern Annular Mode (SAM).
These findings have implications for fisheries management due to the connectivity of early life stages between Chile and the Patagonian Shelf region. Depletion of spawning stock biomass in Chile could impact potential recruitment in the South Atlantic, therefore a co-ordinated management strategy between Chile and the Falkland Islands should be considered
Genetics of gout - Progression from hyperuricaemia to gout
No full textGout is an inflammatory arthritis that is prevalent in New Zealand (NZ) populations, with a higher frequency in Māori (6.06%) and Pacific Islanders (7.60%) in comparison to NZ Europeans (3.24%). This inflammatory arthritis arises from an innate immune response to monosodium urate (MSU) crystals that accumulate in joints and surrounded tissues. MSU crystals are formed in the presence of hyperuricaemia (elevated serum urate levels). Hyperuricaemia (HU) is a prerequisite for gout, but not sufficient. Therefore, it suggests the contribution of other factors that are causal to gout. Genome-wide association studies, an indispensable approach in population genetics, have reported dozens of loci associated with serum urate levels and confirm the importance of urate excretion in controlling urate levels and gout. However, genetic contribution to the progression from hyperuricaemia to gout is poorly understood. Some candidate gene studies have identified genes encoding proteins that are involved in the NLRP3 (NOD-LRR and pyrin domain-containing 3) inflammasome activation that is a key regulator in gout pathogenesis. Thereby, the current research project aims to investigate causal association between non-urate, inflammatory loci and gout.
The current study provides evidence of association between non-urate transporters CNIH2, CUX2, FAM35A and NIPAL1 and inflammatory loci PPARGC1B, IL37 and IL23R with gout in NZ Polynesian and European populations. Recent studies reported association of some of these loci with gout in the Japanese population such as CUX2 (rs4766566), CNIH2 (rs4073582), NIPAL1 (rs11733284), FAM35A (rs7903456), PPARGC1B (rs45520937) and IL23R (rs7517847). The causal role that these variants have in gout pathogenesis in NZ populations has not been reported before and is important for understanding disease mechanisms and developing effective therapeutic stratigies to cure gout.
Population-specific genetic effects on gout are also evident but are not being explored as much as in other complex phenotypes. With the help of an in-silico resequencing approach applied to whole genome sequencing (WGS) gout data, several novel population-specific association signals were found and among these CACNA1S (rs13374149), TAP2 (rs2071) and IL37 (rs17521135) were successfully validated for their association with gout in the New Zealand Polynesian cohort. They were identified with a high prevalence and increasing risk of gout only in a Polynesian sample set. Notably the IL37 (rs17521135) G-allele increased the risk of gout using hyperuricaemic controls compared to gout cases (OR= 1.81, P = 0.031), indicating that this locus is involved in the progression from hyperuricaemia to gout in a population-dependent manner.
Lastly, the current study attempted to evaluate the cause-effect relationship between mitochondria and gout susceptibility through influencing mitochondrial copy number. The hypothesis was generated based on a recent report of identification of low mitochondrial DNA (mtDNA) copy number in Polynesian (Māori and Pacific) gout individuals (Gosling et al. 2018). My study replicated the Gosling et al. (2018) association but did not find association of mtDNA copy number with gout in European. My study evidenced the association of nuclear genome encoded variant rs149132393 (in a FCRL6 gene) with increased mtDNA copy number (in the Eastern Polynesian group) and protected from risk of gout in the Polynesian (Western Polynesian group) population using HU controls versus gout cases. In addition, a previously identified mitochondrial variant 16189C in Polynesian gout patients (Gosling et al. 2018) was associated with gout risk (OR = 0.45, P = 0.045) through mitochondrial-wide association analysis among this NZ Polynesian cohort. Collectively my study indicates a potential contribution of mitochondrial genome variation in gout pathophysiology by affecting mitochondrial copy number
Using non-coding RNAs and proteins to predict acute kidney injury in heart failure
No full textAcute decompensated heart failure (ADHF) is associated with a high incidence of acute kidney injury (AKI), an abrupt loss of kidney function associated with a near doubling of mortality at one year. In addition to the direct threat ADHF itself poses to kidney function, several drugs commonly used to treat HF can exacerbate kidney dysfunction and the beneficial effects of these treatments must be weighed against their adverse effects on glomerular perfusion. Serum creatinine (SCr), the gold-standard marker for glomerular filtration, is a delayed and insensitive marker of kidney function that can delay the diagnosis of AKI by 24-72 hours. During this time, irreversible kidney damage can occur. Consequently, there is an urgent need to identify early markers for AKI and long-term renal impairment in ADHF to facilitate timely implementation of supportive measures to minimise kidney damage and improve patient outcomes.
This project performed a search for novel markers of AKI in ADHF across two classes of potential biomarkers, circulating microRNAs (miRNAs) in patients with ADHF and kidney proteins in an ovine model of renal impairment in ADHF. First, a large-scale screen of 375 miRNAs was performed in a well-phenotyped discovery cohort consisting of ADHF patients who incurred AKI (n=19), and age- and gender-matched ADHF patients who did not incur AKI (n=20), to identify a panel of candidate miRNA markers for AKI in ADHF. Subsequently, circulating concentrations of the 10 most promising candidate miRNAs were measured in 200 consecutively-recruited ADHF patients (with a spectrum of kidney dysfunction) to determine whether any of the candidate miRNAs had potential to provide independent prognostic information beyond established markers such as SCr and markers of ADHF severity including amino-terminal pro b-type natriuretic peptide (NT-proBNP).
Second, kidney tissue samples from an ovine model of ADHF were used to characterise the changes in renal protein expression that occur in response to the development of, and recovery from, renal impairment as a result of ADHF, and identify candidate protein markers of AKI in ADHF. Relative protein quantification was performed in kidney tissue from healthy control sheep (n=5), sheep with established ADHF (n=8) and sheep recovered from ADHF (n=7) using Sequential Window Acquisition of all Theoretical Mass Spectra (SWATH-MS). By investigating associations between candidate miRNA concentrations and AKI, and characterising alterations in renal protein expression in response to development of renal impairment following ADHF, this work aimed to identify clinically useful biomarkers which could be used to identify ADHF patients at risk of AKI.
Key findings from this research included identification of 26 candidate miRNAs which were differentially expressed between patients with ADHF who incurred AKI, and patients with ADHF who did not. Of these candidates, only miR-454-3p validated in a larger, independent cohort. Higher concentrations of miR-454-3p prior to discharge from hospital were associated with lower risk of AKI or intermediate kidney dysfunction in ADHF patients and may add value beyond established risk factors including age in predicting AKI (Odds Ratio 0.58, 95% CI 0.34-1.01, adjusted for ethnicity, age, gender and NT-proBNP). The association between miR-454-3p and AKI was consistent across all major ethnic groups in the validation study (European, Māori and Pasifika), but the study was only sufficiently powered to detect this effect in patients of European ancestry.
Through protein expression profiling, this work identified 189 proteins that were altered > 1.2-fold during the development of and recovery from ADHF in an ovine model. Of these, 11 proteins were detectable in serum, plasma or urine and had a fold-change > 1.2 with an adjusted p-value < 0.05. These included seven candidate protein markers of kidney injury (Filamin A, T-complex protein 1 subunit gamma, Talin 1, Chaperonin containing TCP1 subunit 8, T-complex 1, Crystallin zeta, Peroxiredoxin), one potential protein marker of kidney recovery (Apolipoprotein A4) and three potential protein markers of long-term renal impairment (Apolipoprotein E, Tripeptidyl peptidase 1, Chaperonin containing TCP1 subunit 6A). Of these candidates, eight had never previously been associated with AKI. Differentially expressed proteins were enriched in two pro-inflammatory signalling pathways: the Glycoprotein VI signalling pathway was activated during ADHF development (Z-score 2.65, p< 0.01), and the acute phase response signalling pathway was repressed during recovery from ADHF (Z-score -2.25, p< 0.01).
In conclusion, these findings suggest that miR-454-3p and candidate protein biomarkers, potentially together and in combination with existing clinical risk factors, have the potential to improve detection of AKI, kidney recovery and long-term renal impairment in ADHF. New biomarkers for AKI in ADHF may facilitate targeted treatment and monitoring of patients with ADHF
"Created equal" - A kaupapa Māori analysis of research and health system perspectives of inequity in chronic kidney disease in Aotearoa
No full textUnderstanding Indigenous health inequities requires an equity lens to recognise the impact that colonisation and loss of cultural identity have on health and well-being. An equity lens enables a critical examination and understanding of systems and processes that entrench racism and embed inequity. The United Nations Declaration of the Rights of Indigenous Peoples and Te Tiriti ō Waitangi clearly states that health equity is a basic right of Indigenous Peoples and should form the basis of action in health services and research.
This thesis focuses on chronic kidney disease as a case study to explore and investigate inequities in health outcomes. This thesis includes a critical appraisal of the role of research as a colonisation tool that has maintained health inequity. The thesis explores and enacts Indigenous research praxis, such as Indigenous Data Governance and Sovereignty to assert Indigenous rights, and utilises Indigenous methodology as a tool of decolonisation to explore inequities.
The findings of this thesis led to the design and development of the CONSIDER statement; the Consolidated criteria for strengthening reporting of health research involving Indigenous Peoples. The CONSIDER statement is a consolidation and synthesis of ethics and research guidelines for working alongside Indigenous Peoples, it provides a 17 point checklist for research institutions and researchers by which to record completeness of reporting.
The findings of this thesis present how the use of Indigenous quantitative methodologies has identified significant differences in clinical practice patterns related to Māori experiences of dialysis and transplantation.
This thesis demonstrates that if research and health systems continue along the status quo, without any consideration for roles and responsibilities in relation to health equity, Indigenous Peoples will continue to experience the worst health outcomes in their own nations. Equity in outcomes is not the end goal, elimination of the impacts of colonisation and racism on the health and the long-term well-being of Indigenous Peoples is the end goal. Health research and health systems must continue to strive to address inequities by monitoring the provision of best practice, as well as identifying the provision of future treatment and management practices to ensure equity. Mauri Ora
New Zealand Deprivation Index 2018 - TA52: Nelson City
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/
New Zealand Deprivation Index 2018 - TA62: Selwyn District
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/
New Zealand Deprivation Index 2018 - TA65: Mackenzie District
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/
New Zealand Deprivation Index 2018 - TA68: Waitaki District
No full textFor further information about data sources, interpretation of the graphs, and cautions, please see the separate Introduction Chapter
All data relating to the 2018 census is provided by Stats NZ, https://www.stats.govt.nz/