Publications by authors named "G Lorimer Moseley"

370 Publications

Implicit motor imagery of the foot and hand in people with Achilles tendinopathy: a left right judgement study.

Pain Med 2021 Sep 14. Epub 2021 Sep 14.

La Trobe Sport & Exercise Medicine Research Centre, La Trobe University, Bundoora, VIC, Australia.

Objective: To determine if impairment in motor imagery processes is present in Achilles tendinopathy (AT), as demonstrated by a reduced ability to quickly and accurately identify the laterality (left-right judgement) of a pictured limb. Additionally, this study aimed to use a novel data pooling approach to combine data collected at 3 different sites via meta-analytical techniques that allow exploration of heterogeneity.

Design: Multi site case-control study.

Methods: Three independent studies with similar protocols were conducted by separate research groups. Each study-site evaluated left/right judgement performance for images of feet and hands using Recognise© software and compared performance between people with AT and healthy controls. Results from each study-site were independently collated, then combined in a meta-analysis.

Results: 126 participants (40 unilateral, 22 bilateral AT cases, 61 controls) were included. There were no differences between AT cases and controls for hand image accuracy and reaction time. Contrary to the hypothesis, there were no differences in performance between those with AT and controls for foot image reaction time, however there were conflicting findings for foot accuracy, based on four separate analyses. There were no differences between the affected and unaffected sides in people with unilateral AT.

Conclusions: Impairments in motor imagery performance for hands were not found in this study and we found inconsistent results for foot accuracy. This contrasts to studies in persistent pain of limbs, face and knee osteoarthritis, and suggests that differences in pathoaetiology or patient demographics may uniquely influence proprioceptive representation.
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http://dx.doi.org/10.1093/pm/pnab261DOI Listing
September 2021

Where is my arm? Investigating the link between complex regional pain syndrome and poor localisation of the affected limb.

PeerJ 2021 20;9:e11882. Epub 2021 Aug 20.

IIMPACT in Health, University of South Australia, Adelaide, South Australia, Australia.

Background: Anecdotally, people living with Complex Regional Pain Syndrome (CRPS) often report difficulties in localising their own affected limb when it is out of view. Experimental attempts to investigate this report have used explicit tasks and yielded varied results.

Methods: Here we used a limb localisation task that interrogates implicit mechanisms because we first induce a compelling illusion called the Disappearing Hand Trick (DHT). In the DHT, participants judge their hands to be close together when, in fact, they are far apart. Sixteen volunteers with unilateral upper limb CRPS (mean age 39 ± 12 years, four males), 15 volunteers with non-CRPS persistent hand pain ('pain controls'; mean age 58 ± 13 years, two males) and 29 pain-free volunteers ('pain-free controls'; mean age 36 ± 19 years, 10 males) performed a hand-localisation task after each of three conditions: the DHT illusion and two control conditions in which no illusion was performed. The conditions were repeated twice (one for each hand). We hypothesised that (1) participants with CRPS would perform worse at hand self-localisation than both the control samples; (2) participants with non-CRPS persistent hand pain would perform worse than pain-free controls; (3) participants in both persistent pain groups would perform worse with their affected hand than with their unaffected hand.

Results: Our first two hypotheses were not supported. Our third hypothesis was supported -when visually and proprioceptively encoded positions of the hands were incongruent (. after the DHT), relocalisation performance was worse with the affected hand than it was with the unaffected hand. The similar results in hand localisation in the control and pain groups might suggest that, when implicit processes are required, people with CRPS' ability to localise their limb is preserved.
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http://dx.doi.org/10.7717/peerj.11882DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381877PMC
August 2021

The EPIPHA-KNEE trial: Explaining Pain to target unhelpful pain beliefs to Increase PHysical Activity in KNEE osteoarthritis - a protocol for a multicentre, randomised controlled trial with clinical- and cost-effectiveness analysis.

BMC Musculoskelet Disord 2021 Aug 28;22(1):738. Epub 2021 Aug 28.

Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, The University of Melbourne, Victoria, Australia.

Background: Despite well-established benefits of physical activity for knee osteoarthritis (OA), nine of ten people with knee OA are inactive. People with knee OA who are inactive often believe that physical activity is dangerous, fearing that it will further damage their joint(s). Such unhelpful beliefs can negatively influence physical activity levels. We aim to evaluate the clinical- and cost-effectiveness of integrating physiotherapist-delivered pain science education (PSE), an evidence-based conceptual change intervention targeting unhelpful pain beliefs by increasing pain knowledge, with an individualised walking, strengthening, and general education program.

Methods: Two-arm, parallel-design, multicentre randomised controlled trial involving 198 people aged ≥50 years with painful knee OA who do not meet physical activity guideline recommendations or walk regularly for exercise. Both groups receive an individualised physiotherapist-led walking, strengthening, and OA/activity education program via 4x weekly in-person treatment sessions, followed by 4 weeks of at-home activities (weekly check-in via telehealth), with follow-up sessions at 3 months (telehealth) and 5 and 9 months (in-person). The EPIPHA-KNEE group also receives contemporary PSE about OA/pain and activity, embedded into all aspects of the intervention. Outcomes are assessed at baseline, 12 weeks, 6 and 12 months. Primary outcomes are physical activity level (step count; wrist-based accelerometry) and self-reported knee symptoms (WOMAC Total score) at 12 months. Secondary outcomes are quality of life, pain intensity, global rating of change, self-efficacy, pain catastrophising, depression, anxiety, stress, fear of movement, knee awareness, OA/activity conceptualisation, and self-regulated learning ability. Additional measures include adherence, adverse events, blinding success, COVID-19 impact on activity, intention to exercise, treatment expectancy/perceived credibility, implicit movement/environmental bias, implicit motor imagery, two-point discrimination, and pain sensitivity to activity. Cost-utility analysis of the EPIPHA-KNEE intervention will be undertaken, in addition to evaluation of cost-effectiveness in the context of primary trial outcomes.

Discussion: We will determine whether the integration of PSE into an individualised OA education, walking, and strengthening program is more effective than receiving the individualised program alone. Findings will inform the development and implementation of future delivery of PSE as part of best practice for people with knee OA.

Trial Registration: Australian New Zealand Clinical Trials Registry: ACTRN12620001041943 (13/10/2020).
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http://dx.doi.org/10.1186/s12891-021-04561-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401372PMC
August 2021

The Ebola Virus Interferon Antagonist VP24 Undergoes Active Nucleocytoplasmic Trafficking.

Viruses 2021 Aug 19;13(8). Epub 2021 Aug 19.

Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.

Viral interferon (IFN) antagonist proteins mediate evasion of IFN-mediated innate immunity and are often multifunctional, with distinct roles in viral replication. The Ebola virus IFN antagonist VP24 mediates nucleocapsid assembly, and inhibits IFN-activated signaling by preventing nuclear import of STAT1 via competitive binding to nuclear import receptors (karyopherins). Proteins of many viruses, including viruses with cytoplasmic replication cycles, interact with nuclear trafficking machinery to undergo nucleocytoplasmic transport, with key roles in pathogenesis; however, despite established karyopherin interaction, potential nuclear trafficking of VP24 has not been investigated. We find that inhibition of nuclear export pathways or overexpression of VP24-binding karyopherin results in nuclear localization of VP24. Molecular mapping indicates that cytoplasmic localization of VP24 depends on a CRM1-dependent nuclear export sequence at the VP24 C-terminus. Nuclear export is not required for STAT1 antagonism, consistent with competitive karyopherin binding being the principal antagonistic mechanism, while export mediates return of nuclear VP24 to the cytoplasm where replication/nucleocapsid assembly occurs.
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http://dx.doi.org/10.3390/v13081650DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8402725PMC
August 2021

SARS-CoV-2 suppresses IFNβ production mediated by NSP1, 5, 6, 15, ORF6 and ORF7b but does not suppress the effects of added interferon.

PLoS Pathog 2021 08 26;17(8):e1009800. Epub 2021 Aug 26.

Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.

Type I Interferons (IFN-Is) are a family of cytokines which play a major role in inhibiting viral infection. Resultantly, many viruses have evolved mechanisms in which to evade the IFN-I response. Here we tested the impact of expression of 27 different SARS-CoV-2 genes in relation to their effect on IFN production and activity using three independent experimental methods. We identified six gene products; NSP6, ORF6, ORF7b, NSP1, NSP5 and NSP15, which strongly (>10-fold) blocked MAVS-induced (but not TRIF-induced) IFNβ production. Expression of the first three of these SARS-CoV-2 genes specifically blocked MAVS-induced IFNβ-promoter activity, whereas all six genes induced a collapse in IFNβ mRNA levels, corresponding with suppressed IFNβ protein secretion. Five of these six genes furthermore suppressed MAVS-induced activation of IFNλs, however with no effect on IFNα or IFNγ production. In sharp contrast, SARS-CoV-2 infected cells remained extremely sensitive to anti-viral activity exerted by added IFN-Is. None of the SARS-CoV-2 genes were able to block IFN-I signaling, as demonstrated by robust activation of Interferon Stimulated Genes (ISGs) by added interferon. This, despite the reduced levels of STAT1 and phospho-STAT1, was likely caused by broad translation inhibition mediated by NSP1. Finally, we found that a truncated ORF7b variant that has arisen from a mutant SARS-CoV-2 strain harboring a 382-nucleotide deletion associating with mild disease (Δ382 strain identified in Singapore & Taiwan in 2020) lost its ability to suppress type I and type III IFN production. In summary, our findings support a multi-gene process in which SARS-CoV-2 blocks IFN-production, with ORF7b as a major player, presumably facilitating evasion of host detection during early infection. However, SARS-CoV-2 fails to suppress IFN-I signaling thus providing an opportunity to exploit IFN-Is as potential therapeutic antiviral drugs.
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http://dx.doi.org/10.1371/journal.ppat.1009800DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8389490PMC
August 2021
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