Forced Disruption of Anatomy Education in Australia and New Zealand: An Acute Response to the Covid-19 Pandemic.

Australian and New Zealand universities commenced a new academic year in February/March 2020 largely with "business as usual." The subsequent Covid-19 pandemic imposed unexpected disruptions to anatomical educational practice. Rapid change occurred due to government-imposed physical distancing regulations from March 2020 that increasingly restricted anatomy laboratory teaching practices. Anatomy educators in both these countries were mobilized to adjust their teaching approaches. This study on anatomy education disruption at pandemic onset within Australia and New Zealand adopts a social constructivist lens. The research question was "What are the perceived disruptions and changes made to anatomy education in Australia and New Zealand during the initial period of the Covid-19 pandemic, as reflected on by anatomy educators?." Thematic analysis to elucidate "the what and why" of anatomy education was applied to these reflections. About 18 anatomy academics from ten institutions participated in this exercise. The analysis revealed loss of integrated "hands-on" experiences, and impacts on workload, traditional roles, students, pedagogy, and anatomists' personal educational philosophies. The key opportunities recognized for anatomy education included: enabling synchronous teaching across remote sites, expanding offerings into the remote learning space, and embracing new pedagogies. In managing anatomy education's transition in response to the pandemic, six critical elements were identified: community care, clear communications, clarified expectations, constructive alignment, community of practice, ability to compromise, and adapt and continuity planning. There is no doubt that anatomy education has stepped into a yet unknown future in the island countries of Australia and New Zealand.

Hypothesis: upregulation of a muscle-specific isoform of insulin-like growth factor-1 (IGF-1) by spinal manipulation.

Spinal manipulation is a manual therapy approach commonly employed by chiropractors, osteopaths and manipulative physiotherapists in the treatment of back pain. It is characterised by a rapid high velocity, low amplitude thrust which commonly causes an audible 'pop' or 'cavitation' in the joint. Any beneficial effects are generally explained with reference to changes in vertebral joint movement. This paper looks at the process of spinal manipulation to see if there is reason to expect effects beyond simple changes in the biomechanics of the spine. It shows that during the process of spinal manipulation, rapid stretching of spinal muscles is inevitable. It goes on to review recent evidence that muscle stretch is a potent stimulus for the upregulation of a splice product of the insulin-like growth factor gene by the stretched muscle. Evidence that the product of this gene (mechano-growth factor; MGF) promotes muscle growth and repair (myotrophism) is presented, together with evidence that MGF promotes the growth and repair of neurones (neurotrophism). Against this background the hypothesis is proposed that one of the effects of spinal manipulation is to stretch spinal muscles which will upregulate MGF and result in local myotrophic and neurotrophic effects. This growth factor hypothesis represents a major departure from the biomechanical and biopsychosocial models currently used to explain the effects of spinal manipulation, and could provide the basis for further studies aimed at defining the molecular correlates of this type of manual therapy.

Neuroprotective effect of acute prior inflammation with lipopolysaccharide for adult male rat facial motoneurones.

Increases in inflammatory cytokines are reported to have both neuroprotective and neurotoxic effects depending on the type and age of neurones studied. This study aimed to determine the effect of experimental inflammation induced by Lipopolysaccharide (LPS) on the survival of injured male adult rat facial motoneurones. Time- and dose-response studies were done to optimise the LPS administration time and dose, to best correlate with inflammatory levels previously reported for aged rats. 12 cytokines were assayed through multiplex analysis. 24 h after intraperitoneal injection of 0.5 mg/kg Lipopolysaccharide in rats, IL-1ß, IL-5 and IL-12p70 levels were elevated, with no observed LPS-associated sickness behaviour. In other groups of 5-6 adult rats, the facial nerve was either crushed (as mild injury) or avulsed (as severe injury) after the LPS priming injection. Stereology revealed that most motoneurones survived 28 days after nerve crush only and LPS- or saline-priming preceding nerve crush. Most motoneurones died following nerve avulsion only, whereas over half survived when LPS-priming preceded nerve avulsion. We suggest that elevated levels of experimental inflammation are neuroprotective for severely injured adult male rat facial motoneurones.

Brainstem cytokine changes in healthy ageing and Motor Neurone Disease.

Neuroinflammation is linked to healthy ageing, but its role in the development of age-related neurodegenerative diseases is unclear. In this pilot study we used a multiplex assay approach to compare 27 cytokines in 6 young adult and 6 ageing control brainstems with those in 6 MND brainstems. We report that healthy ageing is associated with significantly increased brainstem levels of IL-1ß, IP-10 and MIP-1ß which co-localise immunocytochemically to astrocytes. MND brainstem is also characterised by a general increase in both pro- and anti-cytokine levels, but fails to show the expected age-related increase in MIP-1ß and IP-10. This pilot study is the first to show that MND is associated with a failure of specific features of the normal age-related neuroinflammatory process. We suggest that our pilot data indicates that neuroinflammation during healthy ageing may not always be detrimental to motoneuronal survival and that age-related neurodegenerative diseases, such as MND, may instead result from defective neuroinflammation.

Different levels of neuroprotection by two insulin-like growth factor-I splice variants.

We compared the neuroprotective effects of a liver-type isoform of insulin-like growth factor-I (IGF-IEa) and its splice variant, mechano-growth factor (MGF), isolated from active skeletal muscle. cDNAs of these peptides were injected into the facial muscle of adult rats prior to facial nerve avulsion. This resulted in significant neuroprotection of 88% and 37%, respectively, of motoneurons compared to control plasmid and avulsion-only groups. MGF is markedly more effective than the liver-type, systemic IGF-I for motoneuron survival, suggesting a major role for the peripheral target in adult neuronal maintenance and survival.

Colorectal and uterine movement and tension of the inferior hypogastric plexus in cadavers.

BACKGROUND: Hypotheses on somatovisceral dysfunction often assume interference by stretch or compression of the nerve supply to visceral structures. The purpose of this study is to examine the potential of pelvic visceral movement to create tension of the loose connective tissue that contains the fine branches of the inferior hypogastric nerve plexus. METHODS: Twenty eight embalmed human cadavers were examined. Pelvic visceral structures were displaced by very gentle 5 N unidirectional tension and the associated movement of the endopelvic fascia containing the inferior hypogastric plexus that this caused was measured. RESULTS: Most movement of the fascia containing the inferior hypogastric plexus was obtained by pulling the rectosigmoid junction or broad ligament of the uterus. The plexus did not cross any vertebral joints and the fascia containing it did not move on pulling the hypogastric nerve. CONCLUSIONS: Uterine and rectosigmoid displacement produce most movement of the fascia containing the hypogastric nerve plexus, potentially resulting in nerve tension. In the living this might occur as a consequence of menstruation, pregnancy or constipation. This may be relevant to somatovisceral reflex theories of the effects of manual therapy on visceral conditions.