29,880 research outputs found
Griffith Climate Action Survey 2023: Summary for Policy and Decision Making
No full textGriffith University’s Climate Action Beacon conducted the third of five planned Climate Action Surveys from September to December 2023. The survey discovered what Australians think, feel, and do about climate change and related environmental and climatic events, conditions and issues. This report gives details of the background of the survey, as well as its methods, major findings and potential implications. Comparisons are made with findings from the corresponding 2021 and 2022 surveys.Full Tex
Playing with Fire: Understanding the Sunni-Shi'a Sectarian Lifecycle
No full textThis article discusses the ingrained impediments which are likely to stifle India's rise and growth - a phenomenon which has figured prominently in scholarly and official assessments, in India and outside, for over a decade now. Intriguingly India's rise as a global power has already been adjudged a certainty in these assessments, but the author contends that there exists an apparent disjuncture between how the world sees India and the prevailing internal impediments. Therefore, any assessment of India as a global power without incorporating these impediments would be incomplete, misplaced and hyperbolic. Of late, in the light of India's growing internal and external socio-economic and political difficulties, more and more writings and proclamations by Indian and international experts indicate emerging scepticism over India's potential as a global power. This paper takes a rollcall of India's internal impediments including, human development, institutional and security challenges which according to the author have already begun restraining India's global ascent.Griffith Business School, Griffith Asia InstituteFull Tex
The Griffith Tax Clinic
No full textGriffith University (Queensland) was one of 10 Australian universities chosen to be part of the 2019 National Tax Clinic Project. This project sought to expand the foundational work done by Curtin University (Western Australia) to establish student tax clinics across Australia. The objectives of these clinics were to provide greater access to justice for unrepresented taxpayers, a rich learning environment for students, and greater tax literacy for the community. The Griffith Tax Clinic opened its doors to the public in July 2019. This article reports on the experience of the Griffith Tax Clinic, in its first year of operation, and sets out key learning outcomes and recommendations gleaned from that experience.Full Tex
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Canyons and Ice: The Wilderness Travel of Dick Griffith
No full textDick Griffith journeyed across Alaska, Canada, Mexico, and the American West. According to Jon Krakauer, "Griffith is simply afflicted with an irresistible inclination to attempt what others say can't be done. When asked what possesses a man to repeatedly strike out alone across hundreds of miles of rugged, lonely country, he replies, 'Every so often, it's just time to walk.'" Kaylene Johnson is author of five books about Alaska including her memoir A Tender Distance: Adventures Raising My Son in Alaska
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
Prediction of Wave-Induced Seabed Maximum Liquefaction Depth Using Artificial Neural Network Model
No full textIn the last few decades, considerable effort has been devoted to the phenomenon of wave-induced liquefaction. In deed, it is one of the most important factors used in analysing
the seabed stability and in designing marine structures. As waves propagate and fluctuate
over the ocean surface, energy is carried within the medium of the water particles. When
this energy is transmitted into the seabed, the results are a rather complex mechanism of
soil behaviours that significantly affect the stability of the seabed.
The prediction of wave-induced seabed liquefaction has been recognised by coastal
geotechnical engineers as an important factor when considering the design of marine
structures. All existing prediction of wave-induced seabed liquefaction models have been
based on conventional approaches of engineering mechanics, with limited laboratory work.
Previous studies have involved complicated procedures and complex mathematical methods.
The present meticulous study has been based on the existing poro-elastic wave-induced
seabed liquefaction solution, and has adopted Artificial Intelligence (AI) technology to
predict maximum wave-induced seabed liquefaction. The author has proposed an alternative
approach for prediction of the maximum liquefaction depth, based on the Artificial
Neural Network (ANN). Unlike previous engineering mechanical approaches, the various
proposed ANN models are based on data learning knowledge, rather than on the knowledge
of the mechanisms. The author has concluded that ANN models can be applicable
to such engineering exercise at least this study.Thesis (PhD Doctorate)Doctor of Philosophy (PhD)Griffith School of EngineeringScience, Environment, Engineering and TechnologyFull Tex
Composing and performing original works for the trombone
No full textThis dissertation explores composing and performing new works for the trombone, and their presentation in a recital designed to demonstrate the potential of the trombone as a soloist instrument. The study builds on the author’s experiences as an orchestral trombonist, as well as his exploration of other styles of trombone playing, including those of brass band and jazz. The author discusses the current repertoire available to trombonists performing recitals, and explores the various qualities of the trombone they demonstrate well. However it goes further to consider what could be done to showcase further its many qualities as a solo instrument. In addition to this artistic research exegesis, the research submission includes the scores of five new compositions by the author featuring a solo trombone, and discusses the process of composing, rehearsing, and performing these works. Their effectiveness in showing off the potential of the trombone as a solo instrument is demonstrated through recordings of live performances of the new works by the author together with colleagues from the Australian National Academy of Music. The research questions posed by the author are addressed through the design and execution of a recital programme that utilises a range of different styles and genres in which the trombone excels. It is proposed that such a programme can potentially showcase more the instrument’s abilities as a solo instrument than is frequently done in traditional trombone recitals.Thesis (Masters)Master of Music Research (MMusRes)Queensland ConservatoriumArts, Education and LawFull Tex
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