A plan development process for solid and hazardous waste management in the Manawatu-Wanganui region: a thesis presented in partial fulfilment of the requirements for the degree of Master of Philosophy at Massey University

This thesis uses elements of the strategic and integrated planning process models to develop a planning process for solid and hazardous waste management for use by a New Zealand regional council. The desired plan outcomes are that: solid and hazardous waste are managed in such a way and at such a rate that the effects on the environment are mitigated and remedied and detrimental effects on the environment are minimised. This outcome should be achieved at a cost which is socially and economically sustainable by the regional community. The scope of the regional plan will also be restricted/ defined by the roles and mechanisms available to regional councils in New Zealand. The philosophy for solid and hazardous waste management is dynamic. The information and technology are generally available. However, action to prevent and mitigate the effects of bad waste management practices relies primarily on planned and coordinated behavioural change. Political will is therefore very important. The plan process chosen reflects the clear ends desired by the plan and the uncertainty over the means needed to achieve that end. Another problem discovered in the course of this research was the lack of integration between planning theory and planning practice. This thesis attempts to bridge that gap by using 'everyday' language

Survival disparities in Indigenous and non-Indigenous New Zealanders with colon cancer: the role of patient comorbidity, treatment and health service factors

Background Ethnic disparities in cancer survival have been documented in many populations and cancer types. The causes of these inequalities are not well understood but may include disease and patient characteristics, treatment differences and health service factors. Survival was compared in a cohort of Maori ( Indigenous) and non-Maori New Zealanders with colon cancer, and the contribution of demographics, disease characteristics, patient comorbidity, treatment and healthcare factors to survival disparities was assessed. Methods Maori patients diagnosed as having colon cancer between 1996 and 2003 were identified from the New Zealand Cancer Registry and compared with a randomly selected sample of non-Maori patients. Clinical and outcome data were obtained from medical records, pathology reports and the national mortality database. Cancer-specific survival was examined using Kaplane-Meier survival curves and Cox hazards modelling with multivariable adjustment. Results 301 Maori and 328 non-Maori patients with colon cancer were compared. Maori had a significantly poorer cancer survival than non-Maori ( hazard ratio (HR) 1.33, 95% CI 1.03 to 1.71) that was not explained by demographic or disease characteristics. The most important factors contributing to poorer survival in Maori were patient comorbidity and markers of healthcare access, each of which accounted for around a third of the survival disparity. The final model accounted for almost all the survival disparity between Maori and non-Maori patients ( HR 1.07, 95% CI 0.77 to 1.47). Conclusion Higher patient comorbidity and poorer access and quality of cancer care are both important explanations for worse survival in Maori compared with non-Maori New Zealanders with colon cancer

A qualitative exploration of the effect of visual field loss on daily life in home-dwelling stroke survivors

Objective: To explore the effect of visual field loss on the daily life of community-dwelling stroke survivors. Design: A qualitative interview study. Participants: Adult stroke survivors with visual field loss of at least six months’ duration. Methods: Semi-structured interviews were conducted with a non-purposive sample of 12 stroke survivors in their own homes. These were recorded, transcribed verbatim and analyzed with the framework method, using an inductive approach. Results: Two key analytical themes emerged. ‘Perception, experience and knowledge’ describes participant’s conflicted experience of having knowledge of their impaired vision but lacking perception of that visual field loss and operating under the assumption that they were viewing an intact visual scene when engaged in activities. Inability to recognize and deal with visual difficulties, and experiencing the consequences, contributed to their fear and loss of self-confidence. ‘Avoidance and adaptation’ were two typologies of participant response to visual field loss. Initially, all participants consciously avoided activities. Some later adapted to vision loss using self-directed head and eye scanning techniques. Conclusions: Visual field loss has a marked impact on stroke survivors. Stroke survivors lack perception of their visual loss in everyday life, resulting in fear and loss of confidence. Activity avoidance is a common response, but in some, it is replaced by self-initiated adaptive techniques

Erratum to A complex intervention to improve pregnancy outcome in obese women; the UPBEAT randomised controlled trial [BMC Pregnancy and Childbirth., 15, (2015), 111], DOI:10.1186/s12884-015-0540-1

Background: Despite the widespread recognition that obesity in pregnant women is associated with adverse outcomes for mother and child, there is no intervention proven to reduce the risk of these complications. The primary aim of this randomised controlled trial is to assess in obese pregnant women, whether a complex behavioural intervention, based on changing diet (to foods with a lower glycemic index) and physical activity, will reduce the risk of gestational diabetes (GDM) and delivery of a large for gestational age (LGA) infant. A secondary aim is to determine whether the intervention lowers the long term risk of obesity in the offspring.<p></p> Methods/Design: Multicentre randomised controlled trial comparing a behavioural intervention designed to improve glycemic control with standard antenatal care in obese pregnant women.<p></p> Inclusion criteria; women with a BMI ≥30 kg/m2 and a singleton pregnancy between 15+0 weeks and 18+6 weeks’ gestation. Exclusion criteria; pre-defined, pre-existing diseases and multiple pregnancy. Randomisation is on-line by a computer generated programme and is minimised by BMI category, maternal age, ethnicity, parity and centre. Intervention; this is delivered by a health trainer over 8 sessions. Based on control theory, with elements of social cognitive theory, the intervention is designed to improve maternal glycemic control. Women randomised to the control arm receive standard antenatal care until delivery according to local guidelines. All women have a 75 g oral glucose tolerance test at 27+0- 28+6 weeks’ gestation.<p></p> Primary outcome; Maternal: diagnosis of GDM, according to the International Association of Diabetes in Pregnancy Study Group (IADPSG) criteria. Neonatal; infant LGA defined as >90th customised birth weight centile.<p></p> Sample size; 1546 women to provide 80% power to detect a 25% reduction in the incidence of GDM and a 30% reduction in infants large for gestational age.<p></p> Discussion: All aspects of this protocol have been evaluated in a pilot randomised controlled trial, with subsequent optimisation of the intervention. The findings of this trial will inform whether lifestyle mediated improvement of glycemic control in obese pregnant women can minimise the risk of pregnancy complications.<p></p&gt

The androgen receptor controls expression of the cancer-associated sTn antigen and cell adhesion through induction of ST6GalNAc1 in prostate cancer

Patterns of glycosylation are important in cancer, but the molecular mechanisms that drive changes are often poorly understood. The androgen receptor drives prostate cancer (PCa) development and progression to lethal metastatic castration-resistant disease. Here we used RNA-Seq coupled with bioinformatic analyses of androgen-receptor (AR) binding sites and clinical PCa expression array data to identify ST6GalNAc1 as a direct and rapidly activated target gene of the AR in PCa cells. ST6GalNAc1 encodes a sialytransferase that catalyses formation of the cancer-associated sialyl-Tn antigen (sTn), which we find is also induced by androgen exposure. Androgens induce expression of a novel splice variant of the ST6GalNAc1 protein in PCa cells. This splice variant encodes a shorter protein isoform that is still fully functional as a sialyltransferase and able to induce expression of the sTn-antigen. Surprisingly, given its high expression in tumours, stable expression of ST6GalNAc1 in PCa cells reduced formation of stable tumours in mice, reduced cell adhesion and induced a switch towards a more mesenchymal-like cell phenotype in vitro. ST6GalNAc1 has a dynamic expression pattern in clinical datasets, beingsignificantly up-regulated in primary prostate carcinoma but relatively down-regulated in established metastatic tissue. ST6GalNAc1 is frequently upregulated concurrently with another important glycosylation enzyme GCNT1 previously associated with prostate cancer progression and implicated in Sialyl Lewis X antigen synthesis. Together our data establishes an androgen-dependent mechanism for sTn antigen expression in PCa, and are consistent with a general role for the androgen receptor in driving important coordinate changes to the glycoproteome during PCa progression

Age standardisation – an indigenous standard?

The study of inequities in health is a critical component of monitoring government obligations to uphold the rights of Indigenous Peoples. In Aotearoa/New Zealand the indigenous Māori population has a substantially younger age structure than the non-indigenous population making it necessary to account for age differences when comparing population health outcomes. An age-standardised rate is a summary measure of a rate that a population would have if it had a standard age structure. Changing age standards have stimulated interest in the potential impact of population standards on disparities data and consequently on health policy

Regional conservation genomics:insights and opportunities from northern Australia

Biodiversity conservation in northern Australia is characterised by high endemism, data deficiency, and high Indigenous land tenure and population. The Northern Australia Conservation Genomics Forum brought together experts to explore current genetic research with particular emphasis on integration of genomics within conservation practices. We discuss the regional biodiversity of northern Australia, highlighting the unique biogeographic patterns, known and unknown species diversity, and ongoing threats such as habitat degradation, altered fire regimes, invasive species, and climate change. This article synthesises key themes from the forum, including the current application of genomics in conservation, gaps and areas of need and opportunity to advance species conservation in this sparsely populated, yet iconic region of Australia. We highlight the need to expand collaborative research partnerships across land tenures with Indigenous organisations, pastoralists, government and non-government organisations, which is crucial for the effective study and conservation of the region’s biodiversity. The paper identifies the challenges and opportunities in applying genomic data to conservation strategies and applied management, including species translocations and habitat management, while acknowledging the limitations and gaps in current research and collections. The insights from this forum emphasise the advantages in using genomics to inform conservation decisions, and the need for continued research and collaboration to protect northern Australia’s unique biodiversity.</p

Tackling health inequalities: moving theory to action

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

SLCO5A1 and synaptic assembly genes contribute to impulsivity in juvenile myoclonic epilepsy

Elevated impulsivity is a key component of attention-deficit hyperactivity disorder (ADHD), bipolar disorder and juvenile myoclonic epilepsy (JME). We performed a genome-wide association, colocalization, polygenic risk score, and pathway analysis of impulsivity in JME (n = 381). Results were followed up with functional characterisation using a drosophila model. We identified genome-wide associated SNPs at 8q13.3 (P = 7.5 × 10−9) and 10p11.21 (P = 3.6 × 10−8). The 8q13.3 locus colocalizes with SLCO5A1 expression quantitative trait loci in cerebral cortex (P = 9.5 × 10−3). SLCO5A1 codes for an organic anion transporter and upregulates synapse assembly/organisation genes. Pathway analysis demonstrates 12.7-fold enrichment for presynaptic membrane assembly genes (P = 0.0005) and 14.3-fold enrichment for presynaptic organisation genes (P = 0.0005) including NLGN1 and PTPRD. RNAi knockdown of Oatp30B, the Drosophila polypeptide with the highest homology to SLCO5A1, causes over-reactive startling behaviour (P = 8.7 × 10−3) and increased seizure-like events (P = 6.8 × 10−7). Polygenic risk score for ADHD genetically correlates with impulsivity scores in JME (P = 1.60 × 10−3). SLCO5A1 loss-of-function represents an impulsivity and seizure mechanism. Synaptic assembly genes may inform the aetiology of impulsivity in health and disease