Publications by authors named "Murielle Kluge"

Background: Variation in stroke treatment metrics highlight a need for approaches to improve clinical processes. Training interventions can improve outcomes, but Australian physician trainees do not currently receive formal process-directed stroke training. Virtual reality (VR) stroke workflow training has proven acceptable, usable, useful and feasible in trial contexts, but how to integrate VR training into physician training remains unclear.

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Background: Stroke management in rural areas is more variable and there is less access to reperfusion therapies, when compared with metropolitan areas. Delays in treatment contribute to worse patient outcomes. To improve stroke management in rural areas, health districts are implementing telestroke networks.

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Background: Psychological stress-related injuries within first-responder organizations have created a need for the implementation of effective stress management training. Most stress management training solutions have limitations associated with scaled adoption within the workforce. For instance, those that are effective in civilian populations often do not align with the human performance culture embedded within first-responder organizations.

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Unlabelled: The use of extended reality (XR) technology in education offers many advantages for transferring knowledge and practical skills training at the higher education level. As a result, many Universities over the past 5 + years have undertaken pilot programs to both develop XR content and assess how to best implement it within existing teaching and learning systems. Unfortunately, very few of these efforts have included structured evaluation or documentation.

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Background: Stroke can be a life-changing event, with survivors frequently experiencing some level of disability, reduced independence, and an abrupt lifestyle change. Not surprisingly, many stroke survivors report elevated levels of stress during the recovery process, which has been associated with worse outcomes.

Purpose: Given the multiple roles of stress in the etiology of stroke recovery outcomes, we aimed to scope the existing literature on stress management interventions that have been trialed in stroke survivors.

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Delays in acute stroke treatment contribute to severe and negative impacts for patients and significant healthcare costs. Variability in clinical care is a contributor to delayed treatment, particularly in rural, regional and remote (RRR) areas. Targeted approaches to improve stroke workflow processes improve outcomes, but numerous challenges exist particularly in RRR settings.

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Background: The precise mechanisms underlying the aetiology of post-stroke fatigue remain poorly understood. Inflammation has been associated with clinically significant fatigue across a number of neurological disorders; however, at present there is a lack of evidence regarding the association of fatigue and inflammation in the chronic phase of stroke recovery.

Aims: The aim of this study was to examine fatigue in a cohort of stroke survivors in the chronic phase of stroke, compared with matched controls, and to explore associations between the pro-inflammatory cytokine interleukin-6, high-sensitivity C-reactive Protein and fatigue.

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Cognitive impairment is a common and disruptive outcome for stroke survivors, which is recognized to be notoriously difficult to treat. Previously, we have shown that low oxygen post-conditioning (LOPC) improves motor function and limits secondary neuronal loss in the thalamus after experimental stroke. There is also emerging evidence that LOPC may improve cognitive function post-stroke.

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This paper describes the conceptual design of a virtual reality-based stress management training tool and evaluation of the initial prototype in a pilot efficacy study. Performance Edge virtual-reality (VR) was co-developed with the Australian Defence Force (ADF) to address the need for practical stress management training for ADF personnel. The VR application is biofeedback-enabled and contains key stress management techniques derived from acceptance and commitment and cognitive behavioural therapy in a modular framework.

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For many chronic stroke survivors, persisting cognitive dysfunction leads to significantly reduced quality of life. Translation of promising therapeutic strategies aimed at improving cognitive function is hampered by existing, disparate cognitive assessments in animals and humans. In this study, we assessed post-stroke cognitive function using a comparable touchscreen-based paired-associate learning task in a cross-sectional population of chronic stroke survivors (≥ 5 months post-stroke, n = 70), age-matched controls (n = 70), and in mice generated from a C57BL/6 mouse photothrombotic stroke model (at six months post-stroke).

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Stroke survivors report significant levels of psychological distress post stroke. To date, most studies conducted have focused on the relationship between psychological stress and functional outcomes in the acute phase of stroke. However, no studies had considered the role of stress over the chronic phase, where stress may continue to exert negative effects on cognitive and psychological processes.

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Introduction: Several studies have shown that stroke survivors report experiencing high and unremitting levels of stress, which can negatively affect brain repair processes and psychological outcomes and thereby compromise recovery. However, it is presently unclear which interventions have been trialled to manage stress in stroke survivors and whether they translate to clinically relevant outcomes. The aim of this scoping review will be to examine stress management interventions in stroke survivors in order to map the types of interventions trialled, commonly reported stress outcome measures and whether a reduction in stress contributes to reductions in relevant clinical outcomes.

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Microglia play a central role in modulating synaptic structure and physiology, learning and memory processes. They exhibit morphological changes to perform these roles, therefore the morphological study of microglia can help to understand their functionality. Many promising methods are proposed to automatically segment the blood vessels or reconstruct the neuronal morphology.

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Automated cell nucleus segmentation is the key to gain further insight into cell features and functionality which support computer-aided pathology in early diagnosis of diseases such as breast cancer and brain tumour. Despite considerable advances in automated segmentation, it still remains a challenging task to split heavily clustered nuclei due to intensity variations caused by noise and uneven absorption of stains. To address this problem, we propose a novel method applicable to variety of histopathological images stained for different proteins, with high speed, accuracy and level of automation.

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It has recently been identified that after motor cortex stroke, the ability of microglia processes to respond to local damage cues is lost from the thalamus, a major site of secondary neurodegeneration (SND). In this study, we combine a photothrombotic stroke model in mice, acute slice and fluorescent imaging to analyse the loss of microglia process responsiveness. The peri-infarct territories and thalamic areas of SND were investigated at time-points 3, 7, 14, 28 and 56 days after stroke.

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Despite the fact that approximately 80% of strokes occur in those aged over 60 years, many pre-clinical stroke studies have been conducted in younger adult rodents, raising debate about translation and generalizability of these results. We were interested in potential age differences in stroke-induced secondary neurodegeneration (SND). SND involves the death of neurons in areas remote from, but connected to, the site of infarction, as well as glial disturbances.

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Background And Purpose: Cognitive impairment is a common outcome for stroke survivors. Growth hormone (GH) could represent a potential therapeutic option as this peptide hormone has been shown to improve cognition in various clinical conditions. In this study, we evaluated the effects of peripheral administration of GH at 48 hours poststroke for 28 days on cognitive function and the underlying mechanisms.

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Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but undamaged by the initial stroke. Our group have published compelling evidence that exposure to psychological stress can significantly exacerbate the severity SND, a finding that has considerable clinical implications given that stroke-survivors often report experiencing high and unremitting levels of psychological stress. It may be possible to use one or more targeted pharmacological approaches to limit the negative effects of stress on the recovery process but in order to move forward with this approach the most critical stress signals have to be identified.

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Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been referred to as secondary neurodegeneration (SND). Using predominantly fixed tissue analyses, microglia have been implicated in regulating the initial response at both damage sites post-stroke.

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Exposure to psychological stress is known to seriously disrupt the operation of the substantia nigra (SN) and may in fact initiate the loss of dopaminergic neurons within the SN. In this study, we aimed to investigate how chronic stress modified the SN in adult male mice. Using a paradigm of repeated restraint stress (an average of 20h per week for 6weeks), we examined changes within the SN using western blotting and immunohistochemistry.

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Exposure to severe stress following stroke is recognised to complicate the recovery process. We have identified that stress can exacerbate the severity of post-stroke secondary neurodegeneration in the thalamus. In this study, we investigated whether exposure to stress could influence the accumulation of the neurotoxic protein Amyloid-β.

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Prestin (SLC26A5) is a member of the SLC26/SulP anion transporter family. Its unique quasi-piezoelectric mechanical activity generates fast cellular motility of cochlear outer hair cells, a key process underlying active amplification in the mammalian ear. Despite its established physiological role, it is essentially unknown how prestin can generate mechanical force, since structural information on SLC26/SulP proteins is lacking.

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