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Sustaining Therapists Assisting Refugee Survivors of Torture and Trauma
Refugees endure cumulative traumatic incidents which deeply affect their sense of safety, identity, support systems, and meaning. When therapists assisting refugees consistently listen to their narratives, they are profoundly impacted. Research highlighting the mutual effects of conflict, war, extreme violence and human rights abuses on both refugee survivors and their therapists is limited. The purpose of this research is to enhance understanding of the impacts of the trials encountered by therapists who assist refugee survivors of torture and trauma, and to contribute towards the development of strategies to support them.
The initial Integrative Review found that existing literature lacked depth and conceptual clarity. The complex experiences of refugee trauma therapists were often oversimplified. A need for deeper exploration was identified.
Guided by these findings the second study, a Photo-elicited Narrative Inquiry was designed to facilitate exploration of underlying processes and to enrich understanding of the lived experiences of refugee trauma therapists. The findings suggested that being forced to re-evaluate familiar belief systems induced intense existential moments.
The secondary analysis which re-analyzed the same dataset from an existential perspective, uncovered intense moments described as ‘a dark night of the soul’, ‘the paradox of life and death’, ‘unhomeliness’, and ‘a falling’. Circumnavigating these concerns influenced how refugee therapists coped with unique work-related challenges.
The follow-up study in which therapists described a challenging work-related situation, identified that therapists drew on a conventional psychotherapy master narrative, consistent with conventional principles of psychotherapy, and an extended psychotherapy master narrative which integrated alternative culturally responsive treatment approaches.
This research recommends establishing peer groups or communities of practice backed by organizational support
Analysing, predicting and improving outcomes for kidney transplant recipients
Kidney failure is a growing global health burden. Kidney transplantation offers the best treatment for eligible patients, however long-term outcomes remain suboptimal due to chronic rejection and premature death, particularly from cardiovascular disease, infection, and cancer. As the transplant population becomes older, more obese, and more comorbid, understanding how these factors influence outcomes is important. Clinical registries and non-inferiority trials are increasingly relied upon to support research and guide policy. This thesis evaluates the reliability of registry data, the impact of evolving transplant population characteristics on outcomes, and the quality of evidence from non-inferiority trials. Deterministic linkage between ANZDATA and the A2309 clinical trial showed excellent agreement for key variables. In recipients aged ≥70 years, transplantation provided a survival benefit beyond 9 months compared to remaining on dialysis. Among 1,522 paired deceased-donor transplants, obesity was associated with higher risks of delayed graft function, graft failure, and death. In 65,712 kidney failure patients, obesity was linked to lower cancer incidence and mortality, with site-specific variation. The systematic review of 44 non-inferiority trials in kidney transplantation identified substantial deficiencies in trial design and reporting, including inadequate justification of non-inferiority margins, inappropriate use of risk measures, poor handling of missing data, and frequent misinterpretation of results. Overall, the ANZDATA Registry provides reliable data for outcome evaluation. Transplantation benefits selected elderly patients despite early risk, while obesity presents complex effects on graft and cancer outcomes. The major deficiencies in non-inferiority trial design and reporting highlight an urgent need for stricter editorial standards, better trialist awareness, and stronger guideline adherence to improve the quality of evidence in our field
Babel, Belonging, and Colonial Queensland (1840–1870): Language, Naming, and the Making of a Colonial Order
This essay is a historical reconstruction rather than a literary interpretation. Between the 1840s and 1870, officials, missionaries, surveyors, and settlers in the colony that became Queensland assembled an Anglophone “language order”: a modular set of practices that distributed belonging and exclusion through interpreting, schoolroom regulation, and naming. David Malouf’s Remembering Babylon serves only as an aperture for the question; the argument rests on administrative records and policy traces.
Methodologically, the essay pairs microhistory with a history of concepts. It reads individual depositions, press notices, and rulebooks alongside survey charts, government gazettes, and mission files, and treats archival guides and indexes not as neutral finding aids but as artefacts of the order under study. Three mechanisms structure the analysis: (1) interpreting and translation as instruments for policing, governance, and evangelisation; (2) classroom language rules that ranked tongues and redirected children’s speech; and (3) onomastic practices of people and places that stabilised spellings and categories for filing, mapping, and search.
Three clusters anchor the case studies: (A) administrative correspondence around Somerset in the 1860s shows how categories and names travelled between London, Brisbane, and Cape York, carrying vernacular labels into official geography; (B) mission schooling and rationing regimes reveal a covert curriculum in which First Languages were discouraged in dormitories and classrooms even as bilingual pupils were enlisted to interpret for order and catechesis; and (C) early translation and grammatical projects in eastern Australia, used here as a comparative lens, expose the politics of nomenclature in paratexts, glossaries, and prefaces, and illuminate Indigenous agency in mediating meanings.
The contribution is twofold. Substantively, the essay recovers how authority moved through routine paperwork such as petitions, rolls, indexes, and gazetteers rather than through a single statute, and explains why the archive still speaks more loudly in some voices than others. Practically, it clarifies the retrieval pathways that continue to govern access today and suggests how indexing, place name restoration, and language programs co-designed with communities can unsettle inherited spellings and categories. Overall, it reframes belonging in colonial Queensland as co-produced through speech governance and naming power.Scholarships & Prizes Office. University of Sydne
Biological effects of pathologies in Lewy body diseases: why timing matters
The emergence of promising biomarkers of α-synuclein Lewy pathology has led to new biological definitions and staging systems for Parkinson's disease and dementia with Lewy bodies. These research frameworks aim to enhance patient selection for studies of biomarkers and disease-modifying therapies. Building on approaches developed for Alzheimer's disease, these new frameworks focus on hallmark neuropathological findings in Lewy body diseases, including abnormal α-synuclein aggregates and neurodegeneration, particularly nigrostriatal dopaminergic loss. Understanding the temporal inter-relationships between Lewy pathology, Alzheimer's disease, and other co-pathologies and symptom manifestation is central to any biological staging system. Neuropathological and in vivo evidence demonstrates substantial temporal and biological heterogeneity in the progression of clinical and pathological events across Lewy body disorders, highlighting knowledge gaps. Staging systems must incorporate this evidence into a nuanced conceptual framework of biological progression. Such revision will be crucial for the appropriate selection of participants and correct timing of targeted interventions in clinical research.Author Accepte
The Death of a Songbird: Listening to Worlds in their (Un)Making
This thesis tells the extinction story of the regent honeyeater (Anthochaera phrygia), a critically
endangered songbird endemic to the forests and woodlands of southeast Australia. Through
attention to the perceived loss of regent honeyeater song, this thesis critically engages with various
epistemic practices within the natural sciences, particularly ecological and ethological literatures, to
explore their world-making effects in the context of endangered-species conservation and extinction.
It considers conservation and research efforts taking place across a variety of forested and
deforested landscapes, as well as in laboratories and zoological gardens. In doing so, this thesis
explores how animal behaviour shapes and is shaped by ecological and social environments,
attending to the various ways in which the social and cultural behaviours of birds, such as song, are
both embodied and emplaced in multispecies contexts. This attention helps us to better hear the
ways in which various humans are implicated in the making and unmaking of species and their
worlds. Ultimately, the stories told throughout this thesis reveal the many worlds contained within a
song and the possibilities and limitations of what may be required in attending to others in a time of
extinctions
An Investigation on the Lipidomic Profile of a Mouse Model of Dravet Syndrome and the Molecular Action of Cannabinoids
Epilepsy is a chronic neurological disorder marked by recurrent seizures, cognitive and motor impairments, and increased mortality. Around 30% of patients are drug-resistant, making it vital to better understand its mechanisms and develop new treatments. Dravet syndrome, a severe developmental and epileptic encephalopathy beginning in infancy, involves persistent seizures, cognitive and behavioural disabilities, sleep problems, and strong resistance to treatment. About 80% of cases are linked to mutations in the SCN1A gene, but much about its underlying biology remains unclear. Evidence suggests lipid dysregulation may contribute to Dravet syndrome, as lipids regulate neuronal activity and are involved in neuroinflammation and the endocannabinoid system. The effectiveness of cholesterol modulators such as soticlestat, the ketogenic diet, and cannabinoids supports this link. However, more research is needed to understand how lipids influence drug-resistant epilepsy and how lipid-like compounds such as cannabinoids act therapeutically.
This thesis investigated the lipid neurochemistry of Dravet syndrome and the pharmacology of cannabinoids. Lipidomic analysis of cortical and hippocampal tissue in Scn1a+/- mouse models revealed lipid profile changes associated with seizure susceptibility. Hexosylceramides emerged as key molecules, showing region- and strain-specific alterations, particularly upregulation in the hippocampus of seizure-prone mice, suggesting disrupted lipid pathways may contribute to seizure vulnerability.
Two cannabinoids, CBC and CBCA, were then examined for their interactions with ABC transporters that regulate brain drug access. Results showed CBCA is an ABCB1 substrate while CBC is not, and neither compound inhibited ABCB1 or ABCG2 activity. Molecular docking confirmed CBCA binding sites on ABCB1, offering insights into cannabinoid pharmacology and their potential as next-generation anti-seizure agents
Investigating Novel Treatments to Improve Radiation Response in Diffuse Intrinsic Pontine Glioma
Diffuse intrinsic pontine glioma (DIPG), now categorised under Diffuse Midline Glioma (DMG) is a fatal paediatric brainstem tumour. Radiotherapy (RT) remains the only effective treatment, however most DIPGs recur due to radioresistance. The hypoxic tumour microenvironment contributes to radioresistance, therefore alleviating hypoxia may improve RT efficacy and patient survival.
We found evidence suggesting increased oxidative phosphorylation (OXPHOS) in DIPG/DMG patient samples suggesting increased oxygen consumption and localised hypoxia. Hypoxia was also validated in DIPG xenografts by positive HIF-1α, VEGFA, and EF5 staining within tumour regions. Hence, we aimed to inhibit OXPHOS to reduce oxygen consumption rate (OCR), alleviate hypoxia and enhance radiosensitivity of DIPG. An anti-parasitic drug screening was performed and atovaquone was identified as the most potent OCR inhibitor. Atovaquone suppressed OCR across multiple DIPG models by targeting complex III, increasing oxidative stress, reducing hypoxia and sensitising DIPG cells to RT. Similar efficacy was observed between commercial and the higher blood-brain barrier (BBB)-penetrant version, amorphous solid dispersion (ASD) atovaquone formulation, supporting evaluation of ASD atovaquone in orthotopic DIPG models. ASD atovaquone demonstrated promising radiosensitising efficacy as it improved survival in orthotopic DIPG model in combination with RT. Mefloquine, another top candidate, inhibited both mitochondrial and glycolytic metabolism, reduced hypoxia and similarly improved radiosensitivity of DIPG cells.
Overall, this thesis provides evidence to support upregulated OXPHOS and the presence of hypoxia in DIPG. Inhibition of OXPHOS with atovaquone and mefloquine alleviated hypoxia and radiosensitised DIPG cells in vitro, with ASD atovaquone showing efficacy in vivo. These findings highlight OXPHOS inhibition as a promising radiosensitising strategy for DIPG and potentially other hypoxic brain tumours
Optimising 99mTc-Pyrophosphate Scintigraphy Acquisition Protocols for Transthyretin Cardiac Amyloidosis Imaging
The use of nuclear imaging in the detection of cardiac amyloidosis, particularly transthyretin (ATTR) amyloidosis, has become an essential aspect of its diagnosis. However, the necessity of imaging at both time points and the optimal time point remains a subject of debate.
This thesis investigates whether SPECT/CT in addition to planar imaging at one hour post injection provides sufficient diagnostic information to potentially eliminate the need for delayed imaging. The project begins with a review of cardiac amyloidosis, its subtypes, diagnostic approaches, and imaging protocols. A systematic literature review explores the diagnostic performance of early versus delayed imaging, focusing on sensitivity, specificity and clinical utility.
Finally, a reader study was conducted in which nuclear medicine physicians independently interpreted single-time-point scans, blinded to the timing of the imaging. Their interpretations were then compared with the original reports which had been generated using both imaging time points. ATTR cardiac amyloidosis was diagnosed based on clinical history, diagnostic test results, electronic medical records, and dual-time-point PYP scan reports. A case was considered positive if the diagnosis or treatment of ATTR cardiac amyloidosis was documented in the medical records.
The findings suggest that an imaging protocol which includes SPECT/CT at the early time point may offer comparable diagnostic accuracy to imaging acquired at both time points. The information provided by the acquisition of SPECT/CT, such as blood pooling and anatomical correlation, is essential for high diagnostic accuracy. The thesis concludes by discussing the implications for clinical practice, highlighting protocol simplification, reduced patient burden, reduced radiation exposure to staff members, and increased departmental efficiency
Noise characterisation of fault-tolerant quantum computers
Noise is the fundamental challenge to quantum computation. Large-scale quantum computers will overcome this challenge with fault-tolerant architectures that leverage quantum error correction. This thesis introduces and investigates a scalable noise characterisation protocol suited to this key context.
First, we introduce this protocol by building upon averaged circuit eigenvalue sampling (ACES), a framework for noise characterisation experiments that simultaneously estimates the Pauli error probabilities of all gates in a Clifford circuit and captures averaged spatial correlations between gates implemented simultaneously in the layers of the circuit. We demonstrate the scalability and performance of our protocol through circuit-level numerical simulations of the entire noise characterisation procedure.
Then we demonstrate in circuit-level numerical simulation that this protocol is practically capable of calibrating a fast correlated matching decoder, enabling noise-aware decoding. We find that noise-aware decoding increases the error suppression factor of the code, leading to reductions in the logical error rate that increase exponentially with the code distance.
Finally, we present several results obtained from experimentally implementing this protocol. We use the noise characterisation results to design an improved syndrome extraction circuit for a heavy hexagon memory that is adapted to the noise characteristics of the quantum device. The model error of our noise characterisation results suggests that the circuit-level Pauli noise model estimated by ACES can describe the essential features of quantum noise. We also operate a heavy hexagon memory and use noise estimates to predict performance and inform decoding.
These results demonstrate that Pauli noise estimates can calibrate decoders to enable noise-aware decoding and inform the co-design of quantum error correcting codes, decoders, fault-tolerant circuits, and quantum devices
Evaluating the effects of a Ketogenic Diet on chemotherapy-induced DNA damage, Cellular Senescence, Apoptosis and chemotoxicity in Acute Myeloid Leukaemia (AML) patients.
Introduction: Acute myeloid leukaemia (AML) is an aggressive blood cancer typically treated with intensive chemotherapy, which non-selectively damages healthy tissues, causing severe side effects. Key treatment challenges include infections, resistance, and relapse, driven by immune-metabolic dysfunction and disrupted DNA damage response (DDR), apoptosis, and senescence. Ketogenic diets (KDs), which reduce glucose availability and enhance immunity, have shown promise in preclinical cancer models, but their role in AML remains unclear.
Aim: This first-in-human study investigates the effects of a KD alongside chemotherapy in newly diagnosed AML patients. It also explores DDR, apoptosis, and senescence- molecular drivers of disease and immune evasion.
Methods: A systematic review/meta-analysis assessed KD effects on insulin-like growth factor 1 (IGF-1), insulin, and glucose. A pilot randomised clinical trial was then conducted in AML patients receiving induction chemotherapy, comparing standard care vs. a KD. Glucose, ketones, and adverse events were monitored. Peripheral blood mononuclear cells were analysed via flow cytometry for DDR (γH2AX, ATM, p-ATM, 53BP1, CHK1 p317), apoptosis (Annexin V/PI), and senescence (p16, p21).
Results: The meta-analysis showed KD reduced IGF-1 by 19.7%, insulin by 29%, and glucose by 6%. KD patients had more stable glucose and elevated ketones during treatment. KD did not affect remission rates. AML blasts from KD patients showed significantly lower DDR markers p-ATM and CHK1 p317. No differences were seen in γH2AX, 53BP1, or ATM. Apoptosis and senescence in blasts were unaffected. In T-cells, KD reduced apoptosis and maintained p-ATM levels during/after chemotherapy.
Conclusion: KD was safe and did not impair remission. It modulated DDR signaling in AML blasts and T-cells, suggesting a dual role—suppressing pro-survival pathways in cancer while protecting immune function. Larger studies are needed to further explore these findings