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30. Health coaching intervention with or without the support of an exercise buddy to increase physical activity of people with chronic low back pain compared to usual care: a feasibility and pilot randomised controlled trial

Author

Fritsch, Carolina G., Ferreira, Manuela L., Halliday, Mark H., Roberts, Katharine, Comachio, Josielli, Mittinty, Manasi, Sharpe, Louise, Foster, Nadine E., Stamatakis, Emmanuel, Mork, Paul J., McLachlan, Andrew J., and Ferreira, Paulo H.

Published
2024
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34. Perceived social support impacts on exercise adherence in patients with chronic low back pain.

Author

Roberts, Katharine E., Ho, Emma, Gassen-Fritsch, Carolina, Halliday, Mark, Mattinty, Manasi Murthy, and Ferreira, Paulo

Subjects
CHRONIC pain treatment, PATIENT compliance, POISSON distribution, PHYSICAL therapy, CHRONIC pain, SELF-efficacy, SECONDARY analysis, EXERCISE, RESEARCH funding, EXERCISE therapy, DISCHARGE planning, DESCRIPTIVE statistics, PAIN management, SOCIAL support, FACTOR analysis, CONFIDENCE intervals, LUMBAR pain, REGRESSION analysis, PHYSICAL activity
Abstract

BACKGROUND: Initiating and maintaining physical activity is particularly difficult for at-risk groups such as those with chronic low back pain (LBP). OBJECTIVE: This study aimed to assess whether there is a relationship between perceived social support (e.g., emotional and physical support) in individuals recently discharged from treatment for chronic LBP and the number of exercise sessions and total amount of exercise they perform over a 6-month period. This study also aimed to investigate a possible mediation effect of exercise self-efficacy on the relationship between perceived social support and exercise adherence (number of exercise sessions and total amount of exercise). METHODS: This prognostic study employed a secondary analysis of data collected for The Buddy Study; Data was collected through online weekly diaries over a 6-month period. Poisson regression analyses were used to quantify the relationship between social support at baseline and total number of exercise sessions, and total amount of exercise performed (frequency and duration) in the 6-month follow-up period. Where a relationship was observed, the Stata SEM command was used for the mediation analysis. RESULTS: A positive relationship was found between participants' perceived levels of social support at baseline and the total number of exercise sessions they performed (IRR = 1.56, 95%CI: 1.18 to 2.06) and the total amount of exercise they performed (IRR = 1.57, 95%CI: 1.05 to 2.35) during the 6-month follow-up period. No mediating relationship was found between exercise self-efficacy at 3-months and the total number of exercise sessions performed (β 3.96, 95% CI: - 4.91 to 12.84), or the total amount of exercise performed (β 243.96, 95% CI: - 258.08 to 746.01). CONCLUSION: Social support is potentially an important aspect of exercise adherence, following discharge from treatment, for those with chronic LBP. People's self-efficacy to exercise does not appear to mediate this relationship. Harnessing social support following physiotherapy treatment may increase exercise adherence and may therefore improve long term outcomes for those with chronic LBP. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Trazodone rescues dysregulated synaptic and mitochondrial nascent proteomes in prion neurodegeneration

Author

Albert-Gasco, Hector, Smith, Heather L., Álvarez Castelao, Beatriz, Swinden, Dean, Halliday, Mark, Janaki-Raman, Sudha, Butcher, Adrian J., Mallucci, Giovanna R., Albert-Gasco, Hector, Smith, Heather L., Álvarez Castelao, Beatriz, Swinden, Dean, Halliday, Mark, Janaki-Raman, Sudha, Butcher, Adrian J., and Mallucci, Giovanna R.

Abstract

The unfolded protein response (UPR) is rapidly gaining momentum as a therapeutic target for protein misfolding neurodegenerative diseases, in which its overactivation results in sustained translational repression leading to synapse loss and neurodegeneration. In mouse models of these disorders, from Alzheimer’s to prion disease, modulation of the pathway—including by the licensed drug, trazodone—restores global protein synthesis rates with profound neuroprotective effects. However, the precise nature of the translational impairment, in particular the specific proteins affected in disease, and their response to therapeutic UPR modulation are poorly understood. We used non-canonical amino acid tagging (NCAT) to measure de novo protein synthesis in the brains of prion-diseased mice with and without trazodone treatment, in both whole hippocampus and cell-specifically. During disease the predominant nascent proteome changes occur in synaptic, cytoskeletal and mitochondrial proteins in both hippocampal neurons and astrocytes. Remarkably, trazodone treatment for just 2 weeks largely restored the whole disease nascent proteome in the hippocampus to that of healthy, uninfected mice, predominantly with recovery of proteins involved in synaptic and mitochondrial function. In parallel, trazodone treatment restored the disease-associated decline in synapses and mitochondria and their function to wild-type levels. In conclusion, this study increases our understanding of how translational repression contributes to neurodegeneration through synaptic and mitochondrial toxicity via depletion of key proteins essential for their function. Further, it provides new insights into the neuroprotective mechanisms of trazodone through reversal of this toxicity, relevant for the treatment of neurodegenerative diseases via translational modulation., Sección Deptal. de Bioquímica y Biología Molecular (Veterinaria), Fac. de Veterinaria, TRUE, pub

Published
2024

38. Targeting the unfolded protein response as a potential therapeutic in prion disease

Author

Halliday, Mark, Mallucci, Giovanna, and McDearmid, Jonathan

Subjects
616.83
Abstract

Many neurodegenerative disorders, including Alzheimer's (AD), Parkinson's (PD) and prion diseases, are associated with the accumulation of misfolded disease-specific proteins. During prion disease, an increase in misfolded prion protein (PrP) generated by prion replication leads to sustained overactivation of the branch of the unfolded protein response (UPR) that controls the initiation of protein synthesis. The UPR is a protective cellular mechanism that is induced during periods of cellular and endoplasmic reticulum stress. UPR activation aims to restore protein homeostasis, by reducing protein translation, and up-regulating chaperone proteins that assist with proper protein folding. However, sustained activation of this pathway results in persistent repression of translation, resulting in the loss of critical proteins that leads to synaptic failure and neuronal death. Inhibiting the UPR by genetic means has recently been shown to be neuroprotective in prion disease (Moreno et al., 2012). A drug screen was performed in the model organism C. elegans to search for inhibitors of the UPR. 34 compounds were identified, of which five were selected for further analysis in C. elegans before being tested as a potential treatment in prion diseased mice. Two compounds, dibenzoylmethane and trazodone hydrochloride displayed efficacy against prion disease, and represent novel therapeutic targets. GSK2606414, a specific inhibitor of PERK (protein kinase RNA-like endoplasmic reticulum kinase), a key mediator of the UPR induced translational repression was also tested in prion diseased mice. It restored protein synthesis and prevented the development of clinical prion disease. These data validate the UPR as a viable target in prion disease, and uncover promising potential therapeutics.

Published
2014

39. Errata

Author

Halliday, Mark

Subjects
Errata (Halliday, Mark) (Poem), Arts, visual and performing, Literature/writing
Abstract

In stanza 7, read evening instead of craving: After lingering as if wistfully above the live-oaks along the park's west side, the red sun suddenly plunged from sight to quench [...]

Published
2023

44. My Continuity

Author

Halliday, Mark

Subjects
My Continuity (Poem), Arts, visual and performing, Literature/writing
Abstract

That day in 19741 sat in the sun in the small back yard of the brown house on Elmgrove Avenue with a pile of books on the chair beside me, [...]

Published
2023

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