150,302 research outputs found
Panoramic view looking north over the mouth of Granite Harbour, Cape Geology, Antarctica, ca. 1911 [picture]/
No full textTitle devised by cataloguer based on information from acquisition documentation.; Part of the Professor Griffith Taylor collection.; Condition: Some lifting of the emulsion along left edge.; "Panorama looking N. mouth of Granite Harbour GT"--Information from acquisition documentation.; Also available in electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4459165
Griffith Climate Action Survey: Summary for Policy and Decision Making
No full textThe Griffith Climate Action Beacon (CAB) seeks to develop knowledge, leadership, capacity, and responses to enable effective and just action throughout society, with a focus on interdisciplinary research and cross-sectoral practice collaborations as catalysts for change. A key point of difference from other facilities is that the CAB’s interdisciplinary and partnership approach enables research disciplines and communities-of-practice to collaboratively define, research, implement, and evaluate solutions for climate action.Full Tex
Chronic Inflammation: A Link Between Cardiometabolic and Mood Disorders?
No full textWe live in an age of 'multimorbidity', yet have a rather poor understanding of the impacts of this phenomenon from cellular to organ and system levels. Bi-directional relationships are observed between cardiometabolic (diabetes mellitus, coronary heart disease) and mood disorders (major depressive disorder), each increasing disease risk and frequently co-existing. This cardiometabolic-mood interaction may reflect an under-appreciated commonality of underlying mechanisms across these pathologies. Importantly, comorbid development of these disorders exacerbates the already profound burdens of these individual chronic disorders. Further, psychosocial stress and ageing – increasingly prevalent features of modern societies - may promote these conditions and worsen outcomes. In assessing the intersections of these inter-related disorders, chronic low-grade inflammation is often highlighted and implicated as a common early substrate in cardiometabolic and mood disorders, linking these dominant diseases. Nonetheless, how immunoinflammatory dysregulation drives multimorbidity, and influences 'multifinality' (diverse disease outcomes from common risks/causes), are unclear. Whether immunoinflammatory changes in metabolic vs mood disorders are unique or involve common motifs, and how these interact in dictating cardiometabolic and mental health, remains to be established. Dysregulation of toll-like receptor (TLR) signalling has been specifically implicated in these diseases, potentially presenting a mechanistic nexus in comorbid development of cardiometabolic and mood disorders.
The doctoral work presented in this thesis was designed to address the broad concept of mechanistic intersections contributing to rising multimorbidity. In order to practicably achieve this at a systems level, four major tissues impacted by and contributing to aspects of metabolic and mood disorders were studied: the brain, heart, liver and blood (circulating serum). The brain is an overarching and critical organ, regulating both mood and metabolic homeostasis, and influencing all other organ systems. Cardiac tissue is assessed as it is particularly impacted by type 2 diabetes (T2D); the risk of cardiovascular disease (CVD) is markedly elevated in T2D patients and is the lead cause of death in these patients. Further, CVD is an independent risk factor for both depression and T2D. The liver is fundamental to metabolic homeostasis (the central organ maintaining homeostasis across fed and fasted states via oxidisable substrate storage and release), links the gut to the periphery (gut-liver axis) and contains specialised macrophages which are front-line responders to gut-derived lipopolysaccharides (LPS) (arising with gut permeability changes). Finally, serum was assessed as it is the primary medium for transport of macronutrients, hormones and immunoinflammatory molecules throughout the body.
To avoid the pitfalls of reliance upon gene-modified animal models, non-genetic murine models of type 1 and type 2 diabetes development in early adulthood were studied in Chapter 2 to explore potential changes in TLR-related signalling at the gene level. Somewhat unexpectedly, there was little evidence of shifts in TLR signalling in central nervous system (CNS), hepatic or cardiac tissues in these two conditions. Moreover, while modest elevations in circulating interleukin-6 (IL-6) are observed in T2D animals, tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) levels remained unchanged across models. Together with further analysis of gene expression, these data indicate that the T2D model does not develop an overtly pro-inflammatory phenotype, despite clear evidence of metabolic dysregulation. Given that a well-developed diabetic phenotype was observed (increased body weight, moderate hyperglycaemia, insulin resistance), this work called into question the essential role of TLR4 in the pathogenesis of T2D. Data does reveal marked changes in circulating adipokines and catecholamines, suggesting these endocrine systems may be key to disease progression, independent of inflammation. Surprisingly, assessment of circulating LPS revealed serum levels were decreased (although not significantly) in T2D animals, which casts doubt on whether 12 weeks of feeding with a ‘Western diet’ (30% of total calories from fat) is sufficient to disturb gut physiology and trigger the systemic innate immune response. The majority of animal models employ much higher fat percentages (45-60% calories from fat) in their diabetogenic diets, despite such high fat levels vastly exceeding those in a Western diet (~30%) and raising questions of pathophysiological relevance. Given that little evidence of TLR dysregulation was detected at a physiologically relevant fat percentage, a more chronic model (21-week dietary modification) with an intermediate fat content (43% calories from fat) was developed for subsequent experimentation.
Studies in Chapter 3 demonstrate that a more profound weight gain is achieved with a higher fat content, which still remains below the extreme 60% levels often studied in animal models: this new feeding regime resulted in significantly greater body weight gain although fasting insulin and glucose levels were not altered when compared with the T2D model assessed in Chapter 2. Nonetheless, despite this more pronounced phenotype, limited TLR4-related gene changes were observed in the model. Selective changes to total cellular nuclear factor-kappa B (NF-κB) protein expression were observed in hepatic tissue, although analysis of the nuclear compartment revealed no changes in response to T2D. Thus, while a greater pool of this critical pro-inflammatory factor was evident, this was not necessarily associated with increased nuclear interaction and thus transcriptional control. These data suggest dysregulation of transcriptional control by NF-κB (particularly TLR4 pathway elements) may not be essential in the evolution of T2D in these animals.
Examining a dietary intervention with an omega-3 polyunsaturated fatty acid (n-3 PUFA), α-linolenic acid (ALA), which has been linked to anti-inflammatory outcomes in some chronic disorders, revealed no improvements in the systemic sequalae of T2D. This is consistent with evidence PUFA supplementation may (somewhat paradoxically) have greater influences on metabolic homeostasis in healthy rather than diseased subjects. Unexpected elevations in key inflammatory transcripts were noted with ALA supplementation, potentially reflecting the highly pleiotropic actions of PUFAs. Proteomic profiling of cardiac tissue revealed that a number of inflammatory and related factors beyond TLR-related signalling were impacted by T2D (Serpin-1/PAI-1, leptin, resistin) and/or are sensitive to ALA (IL-10, CD40, VEGF). Data also suggest animal age may be a complicating factor in the protracted disease model, producing apparent independent effects on leptin/insulin expression levels, in turn complicating interpretation of these data. Finally, specific investigation of CNS changes in the model - via analysis of frontal cortex (FC) leptin receptor expression - indicates a sensitivity of central leptin signalling to T2D, which may not only participate in metabolic dysregulation but behavioural outcomes (as suggested in the pathogenesis of depression, for example). This highlights the likely importance of central control and behavioural determinants of disease outcomes.
Investigating central control mechanisms and behaviour in more detail, studies presented in Chapter 4 revealed that the T2D phenotype involves induction of anxiety-related behaviours without impacting on hedonic behaviour. Further, despite evidence from other studies of the benefits of PUFA supplementation in mood disorders, ALA supplementation did not reverse anxiety-related behaviours, though increased locomotion in both healthy and T2D animals. Interestingly, analysis suggests ALA supplementation may confer benefits to locomotive activity independently of disease state, although outcomes are better in healthy controls. Examining elements of central reward pathways, neurotransmission, endocrine and inflammatory control in FC and hippocampus revealed select changes with T2D, including elevated Drd2 (dopamine D2 receptor) and reduced Htr1a (serotonin receptor 1A) in the FC, together with shifts in leptin receptor expression. Surprisingly, hippocampal Il1b gene expression remained similar between groups, though this is consistent with no change in hedonic behaviour. Circulating dopamine and leptin were also sensitive to T2D, with hippocampal dopamine levels selectively elevated in T2D animals supplemented with ALA (although the relevance of this finding is not clear). Overall, these data point to dysregulation of central dopamine and leptin signalling, which may contribute to behavioural disruption in T2D, in turn influencing disease development and outcomes.
In the final studies, CNS responses were explored in greater detail via RNA-sequencing (Chapter 5), more broadly testing whether metabolic and mood disorders share common nervous system changes. Analyses of transcriptome profiles in the FC of the T2D model assessed in Chapter 5 together with a model of chronic social stress (SS) known to induce anxiety/depressive behaviours again provided limited support for an overarching immunoinflammatory dysregulation as a key driver of behavioural changes. These analyses reveal both distinct and common processes (beyond TLR-signalling) that are dysregulated in disease. Comparison between T2D and SS models reveal commonalities in CNS leptin and insulin receptor changes, congruent with evidence of insulin and leptin resistance in the T2D model and their implication in both human major depressive disorder (MDD) and T2D. A majority of over-represented genes were related to cell/tissue development, cell migration and proliferation, suggesting a dominant role for CNS 'remodelling' with both metabolic and mood disorders. Interestingly, down-regulation of ATP metabolic processes and mitochondrial genes was evident in the SS model but not T2D, supporting a more dominant effect of stress on energy production.
Taken together, the findings presented in this doctoral project raise questions regarding the role of dysregulated TLR-signalling in T2D (and stress-related disorders). Despite a clear diabetic phenotype and shifts in behavioural profiles of T2D animals, findings challenge whether TLR-related dysregulation (reported by others) may be a consequence rather than causative factor in disease pathogenesis. Importantly, evidence is presented that insulin, leptin and dopamine signalling (together with other metabolic mediators) may be important linkages between metabolic and mood disorders, and underlie behavioural detriment in T2D. In terms of limiting the development or impacts of disease, n-3 PUFA supplementation resulted in selective benefits in T2D, though these appear unrelated to the metabolic profile of these animals. Finally, shared and unique CNS changes were identified in models of T2D and chronic social stress, supporting structural sensitivity and plasticity with inter-related metabolic and mood disorders.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)School of Medical ScienceGriffith HealthFull Tex
Trimethylamine-N-oxide in the Healthy and Diseased Heart
No full textCardiovascular disease (CVD) remains the greatest cause of death globally, despite ongoing efforts to prevent disease and optimise clinical therapies. The development of CVD is largely dependent on lifestyle risk factors prevalent in modern societies, including poor diet and exercise habits, smoking status, low socioeconomic status, and psychosocial stresses. A lifestyle of chronic unhealthy eating habits, together with these factors, drives common metabolic disorders such as type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS), both strongly contributing to the risk of CVD. Over recent decades, a growing body of literature identifies and supports a key role for the gut microbiome in the aetiology of our most common chronic diseases, including CVD. Indeed, dietary factors not only governs overall energy balance, but influences the gut microbiome. In particular, the gut microbial metabolite trimethylamine-N-oxide (TMAO) has been identified as a potential player in the linkages between diet, the gut microbiome, and CVD development and outcomes.
Elevations in circulating TMAO have been observed in chronic (often comorbid) disorders such as obesity, T2DM, heart failure and chronic kidney disease, as well as in advanced age. Additionally, studies using in vitro and in vivo models indicate that TMAO may well promote CVD, enhancing atherosclerotic disease via stimulatory effects on inflammation and oxidative stress. Despite considerable ongoing investigations, some fundamental questions remain unaddressed. Critically, the TMAO concentrations commonly used to induce and study such pathological outcomes are generally many-fold higher than observed in human disorders, and animal models of disease. In addition, it is not clear whether TMAO can induce pathology in otherwise healthy people, in the absence of co-morbidities. Findings are conflicting in this regard, thus it remains to be established whether TMAO actively drives disease or represents a potentially useful biomarker secondary to evolving cardiometabolic disease. In terms of cardiovascular influences, most in vitro and in vivo studies focus on vascular and inflammatory effects, with much less information available regarding both myocardial and also mitochondrial effects of TMAO. The latter mitochondrial dysfunction is broadly implicated in common cardiometabolic diseases. Given these unknowns, and gaps in the literature regarding TMAO in CVD, this doctoral project sought to establish whether extracellular concentrations of TMAO observed in mild and severe cardiovascular or related metabolic diseases are sufficient to independently impact the heart, its vessels, and myocardial mitochondria. Questions addressed include whether cardiovascular effects are evident with acute elevations in TMAO or require chronic changes; do such effects emerge in otherwise healthy hearts or are they more evident in extant disease; and, what are the relationships between TMAO concentrations, cardiometabolic risk factors, diet, and gut microbiome profile. […]Thesis (PhD Doctorate)Doctor of Philosophy (PhD)School of Pharmacy & Med SciGriffith HealthFull Tex
An Improved Technique for Estimating Plant Available Nitrogen Supply from Recycled Organic Wastes Applied to Agricultural Land
No full textIn order to integrate organic fertilisers into mainstream agriculture, it is necessary to be able to predict with reasonable accuracy the supply of nutrients from a given product. This will allow organic fertilisers to be applied to the soil at correct rates (on their own and in combination with inorganic fertilisers) to meet the crop nutrient requirements and avoid any excess supply that might harm the environment. The focus of the research within this thesis was on the supply of plant available nitrogen (PAN) from recycled organic (RO) wastes and its prediction. The research documented in this thesis addressed the following four hypotheses; • Hypothesis 1 – The NLBAR (i.e. Nitrogen Limited Biosolids Application Rate) formula (New South Wales biosolid guidelines) and its percentage organic N mineralisation assumptions provide an accurate prediction of the mineral N supply from biosolids in the first year of a crop. • Hypothesis 2 – RO waste composition affects the proportion of its organic N mineralised in the soil. • Hypothesis 3 – Certain composition characteristics of RO wastes can provide a reliable prediction of the mineral N supply from RO wastes under controlled conditions. • Hypothesis 4 – Near-infrared spectrometry can be used to accurately predict the mineral N supply and recalcitrant C pools from RO wastes applied to the soil, under controlled conditions.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)Griffith School of EnvironmentScience, Environment, Engineering and TechnologyFull Tex
Nitrous Oxide Emissions from Vegetable Cropping Systems
No full textAgricultural manipulation of the soil nitrogen (N) cycle has caused a significant increase in nitrous oxide (N2O) emissions during the past five decades. Nitrous oxide is one of the major greenhouse gases with potent and long-lasting global warming effects [298 times higher than carbon dioxide (CO2) over a time period of 100 years]. The major biogenic processes responsible for N2O production in agricultural soils are identified as nitrification which is the oxidation of ammonium (NH4+) to nitrite (NO2-) and nitrate (NO3-) and denitrification that is the anaerobic reduction of NO2- and NO3- to gaseous nitric oxide (NO), N2O or N2. Although the current concentration of N2O in the atmosphere is relatively lower than other greenhouse gases, it is annually increasing at a rate of 0.25%. Vegetable cropping systems, a major agricultural activity worldwide, generally comprise intensive cultivation and high rates of N application. However, the N recovery from intensively cultivated vegetable fields is reported to be only 20 - 50% of the applied N fertiliser, suggesting large amounts of N loss from these fields. In Australia, horticulture represents less than 1% of land used for agriculture, but accounts for 6-12% of N fertiliser use in agriculture and its contribution to national N2O emissions is significant.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)Griffith School of EnvironmentScience, Environment, Engineering and TechnologyFull Tex
Residue Management and Carbon and Nutrient Cycling in Exotic Pine Plantations of Southeast Queensland
No full textIn Southeast Queensland, Australia, future wood production from exotic pines will rely heavily on second-rotation plantations. This increases the importance of sustaining soil fertility through logging or harvest residue retention for soil organic matter (SOM) maintenance in forest plantations. However, a greater understanding of harvest residues and their impact is essential to fully realise the potential of harvest residue management as an integral component of sustainable production forestry. Therefore, this study examined the nature of harvest residues, their decomposition and nutrient release dynamics, and the short- and long-term impacts of the residues on soil carbon (C), nitrogen (N) and phosphorous (P) pools, tree nutrition, growth and productivity in exotic pine plantations of Toolara State forest (26 degrees 00' South, 152 degrees 49' East), Maryborough districy, southeast Queensland.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)Griffith School of EnvironmentScience, Environment, Engineering and TechnologyFull Tex
Temporal and Spatial Variations in the Abundance of Soil Denitrifying Bacteria in Australian Sclerophyll Forests: Effects of Prescribed Burning
No full textNearly one fifth of Australia’s continent is covered by forests, including 147.4 million hectares of native forest and 2.0 million hectares of forestry plantations. Australia has about 4 percent of the world’s forests on 5 percent of the world’s land area. Prescribed burning has been extensively applied to manage forest fuels in Australia since the 1960s. It greatly decreases the wildfire hazard, promotes forest regeneration and controls insects and disease. Fire modifies both the above-ground vegetation and below-ground microbial community. Despite the significant role of prescribed burning in nitrogen (N) dynamics, most studies have focused only on the responses of one or several forest components (e.g. vegetation, microbial community or soil nutrients) to fire separately. Few studies have offered an in-depth insight into the relationship between soil N cycling processes and associated functional communities in response to long-term prescribed burning.
Denitrification is an important part of forest N cycling. It is a stepwise dissimilative reduction process of nitrate (NO3-) to dinitrogen gas (N2) under anaerobic conditions and the primary pathway of nitrous oxide (N2O) emission from soil. This gaseous product has a global warming potential about 298 times greater than that of carbon dioxide (CO2). The potential environmental implication of denitrification to global warming has drawn increasing scientific attention worldwide. A variety of microbial functional groups participate in the denitrification process and each of them can be measured by targeting one or more specific functional genes.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)Griffith School of EnvironmentScience, Environment, Engineering and TechnologyFull Tex
The link between product market reform and macro-economic performance
No full textValue-added per capita in EU countries has lagged behind the US. This is despite widespread reforms to product markets across EU countries aimed at increasing growth. This study analyses the macro-economic impact of product market reforms undertaken in the European Union over the 1980s and 1990s by examining a large number of regulations and reforms across EU countries.product market, product market reforms, regulations, macro-economic performance, allocative efficiency, productive efficiency, dynamic efficiency, aggregate economy, Griffith, Harisson
The health and economic impact and cost-effectiveness of interventions for the prevention of overweight and obesity in Kenya: a stakeholder engaged modelling study
No full textGlobally, overweight and obesity have been identified as leading risk factors for noncommunicable diseases (NCDs). In Kenya, the increasing prevalence of overweight and obesity and related NCDs has created a double burden of disease due to the persisting burden of infectious diseases. There are multiple potentially effective strategies for the prevention and control of overweight and obesity. It is important to ensure that choice of interventions leads to optimal health for the available budget. Health impact assessment and cost effectiveness analysis of interventions provide evidence to guide such policy decisions. This thesis aims to assess the health and economic impact of overweight and obesity in Kenya and assess the impact and cost-effectiveness of interventions for the prevention of overweight and obesity in Kenya.
The thesis applies the Assessing Cost-Effectiveness (ACE) approach to priority setting with stakeholder engagement as part of the due process. The Kenya Obesity Model, a proportional multistate life table model was developed and used to conduct three assessments. In the first assessment, the future course of the population disease burden in Kenya that is attributable to high body mass index (BMI) is modelled, against an upward trend in BMI. This is implemented by estimating the impact of the elimination of exposure to high BMI (>22.5kg/m2) on health adjusted life years, health adjusted life expectancy, and the burden of 27 obesity-related diseases. In the second assessment, the potential impact of achieving Kenya’s set obesity target (halting the rise of overweight, including obesity, by 2025) is quantified. Outcomes assessed include the impact on health, healthcare costs and productivity gains. The Human Capital Approach to estimate productivity gains. In the third assessment the potential health impact, economic impact, and cost-effectiveness of interventions for the prevention and control of overweight and obesity in adults in Kenya is estimated. Interventions for inclusion were selected from two broad strategies identified by stakeholders. Considering a health system perspective, two interventions were assessed for cost-effectiveness. Incremental cost-effectiveness ratios (ICERs) were calculated. The Human Capital Approach was used to estimate productivity gains.
For all the three assessments, the 2019 Kenya population was modelled over their remaining lifetime with risks for the related NCDs rising only from age 20 and no burden among children. Within the model, the productivity outcomes are estimated for the 2019 working population in Kenya (20 years up to retirement age of 65 years) over their lifetime. Deterministic and probabilistic sensitivity analyses were conducted to quantify uncertainty.
Findings showed that elimination of high BMI could see approximately 83·5 million health-adjusted life years (HALYs) saved, and the health-adjusted life expectancy increased by 2·3 (95% uncertainty interval [UI] 2·0-2·8) years for females and 1·0 (95% UI 0·8-1·1) years for males. Halting the rise of overweight in the year 2025 was estimated to save 6.8 million HALYs (95%UI 5.8- 7.9 million) over the lifetime of the 2019 Kenyan population or 135 HALYs per 1,000 persons. About US 15 per capita) equivalent to 16% of Kenya’s current annual healthcare
expenditure. The total productivity gains resulting from a reduction in obesity-related mortality and morbidity (combined) could be as high as ~US$ 5.8 billion by 2044. When interventions were evaluated, the findings show that all modelled interventions would yield substantial health gains, healthcare cost savings and productivity gains. There were wide differences in the sizes of the impacts, with two specific interventions (a 20% tax on sugar-sweetened beverages and mandatory kilojoule menu labelling) resulting in good impact while two more broad scenarios that were assumed to results in large changes in consumption patterns had very large impacts (i.e., a change in national consumption levels scenario and a change in consumption levels related to supermarket food purchase). The two interventions were found to be very cost effective without cost offsets, and dominant (health promoting and cost-saving) with cost offsets included. These interventions could be considered for implementation as part of Kenya’s NCD control plans.
The magnitude of the health and economic impact of overweight and obesity in Kenya underscores the need to prioritise prevention and control of overweight and obesity and related NCDs in Kenya. The Kenya Obesity Model infrastructure can be used in future research work to help set priorities for NCD control in Kenya and similar settings.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)School of Medicine & DentistryGriffith HealthFull Tex
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