Immersive learning: Enhancing student engagement using 360° photography and unity simulations in undergraduate medical science courses

Student engagement is a crucial factor that can influence both the student learning experience and student success. However, in response to the recent COVID-19 pandemic, learning for tertiary students had been affected as many universities introduced fully online learning. This shift to online learning has had an adverse effect on engagement for many students. Immersive online learning modules, including interactive simulations, have potential to enhance motivation and engagement. This study aimed to compare existing online standard module lessons (2D virtual laboratory spaces) with platforms and conditions that apply immersive virtual learning environments (360o photography and desktop Unity 3D immersive simulations) and evaluate the effects on the student learning experience and performance. Novel virtual learning environments were created to pilot within a third-year undergraduate pathology course, at the University of New South Wales. The study was conducted using a multimodal approach with two different pathology undergraduate cohorts from 2022 to 2023. Each cohort was randomly divided into two groups to trial a different learning environment. In 2022, we compared an existing online standard module (developed using a HTML platform, H5P) with a 360o laboratory space. In 2023, we compared the existing standard online module with an immersive 3D Unity laboratory simulation. Student engagement and performance was assessed across all learning environments using pre- and post-simulation knowledge/transfer tests, and Qualtrics feedback surveys. Qualitative and quantitative data obtained were used to compare factors such as student motivation, engagement, and confidence within the different learning environments. In feedback surveys, students reported being engaged and immersed in both the 360o environments and in the 3D Unity simulations. However, students also reported navigation issues within the virtual learning environments in addition to reporting cognitive overload. Quantitative data revealed an increase in performance on knowledge/transfer tests regardless of the learning environment type, but the level of improvement between each group was not significantly different. Further data revealed an overall improvement in understanding of content for all learning environments, but there was a greater increase with the standard module groups. This could be attributed to possible cognitive overload experienced within the new virtual learning environments. As reported in this study, despite the engaging/immersive properties of the 360o/Unity environments, newly developed learning simulations may overload or distract the learner. Therefore, further work is required on immersive learning environment factors that promote student engagement and motivation. These promoting factors could also be incorporated into face-to-face learning so that key elements for student engagement are aligned in all learning environments

Early-life viral infection and allergen exposure interact to induce an asthmatic phenotype in mice

<p>Abstract</p> <p>Background</p> <p>Early-life respiratory viral infections, notably with respiratory syncytial virus (RSV), increase the risk of subsequent development of childhood asthma. The purpose of this study was to assess whether early-life infection with a species-specific model of RSV and subsequent allergen exposure predisposed to the development of features of asthma.</p> <p>Methods</p> <p>We employed a unique combination of animal models in which BALB/c mice were neonatally infected with pneumonia virus of mice (PVM, which replicates severe RSV disease in human infants) and following recovery, were intranasally sensitised with ovalbumin. Animals received low-level challenge with aerosolised antigen for 4 weeks to elicit changes of chronic asthma, followed by a single moderate-level challenge to induce an exacerbation of inflammation. We then assessed airway inflammation, epithelial changes characteristic of remodelling, airway hyperresponsiveness (AHR) and host immunological responses.</p> <p>Results</p> <p>Allergic airway inflammation, including recruitment of eosinophils, was prominent only in animals that had recovered from neonatal infection with PVM and then been sensitised and chronically challenged with antigen. Furthermore, only these mice exhibited an augmented Th2-biased immune response, including elevated serum levels of anti-ovalbumin IgE and IgG₁as well as increased relative expression of Th2-associated cytokines IL-4, IL-5 and IL-13. By comparison, development of AHR and mucous cell change were associated with recovery from PVM infection, regardless of subsequent allergen challenge. Increased expression of IL-25, which could contribute to induction of a Th2 response, was demonstrable in the lung following PVM infection. Signalling via the IL-4 receptor α chain was crucial to the development of allergic inflammation, mucous cell change and AHR, because all of these were absent in receptor-deficient mice. In contrast, changes of remodelling were evident in mice that received chronic allergen challenge, regardless of neonatal PVM infection, and were not dependent on signalling via the IL-4 receptor.</p> <p>Conclusion</p> <p>In this mouse model, interaction between early-life viral infection and allergen sensitisation/challenge is essential for development of the characteristic features of childhood asthma, including allergic inflammation and a Th2-biased immune response.</p

Altered expression of microRNA in the airway wall in chronic asthma: miR-126 as a potential therapeutic target

Background: The role of microRNAs (miRNAs) in regulating gene expression is currently an area of intense interest. Relatively little is known, however, about the role of miRNAs in inflammatory and immunologically-driven disorders. In a mouse model, we have previously shown that miRNAs are potentially important therapeutic targets in allergic asthma, because inhibition of miR-126, one of a small subset of miRNAs upregulated in the airway wall, effectively suppressed Th2-driven airway inflammation and other features of asthma. In the present study, we extended investigation of the therapeutic potential of miRNA inhibition to our well-established model of chronic asthma. Methods: Female BALB/c mice were systemically sensitised with ovalbumin (OVA) and chronically challenged with low mass concentrations of aerosolised OVA for up to 6 weeks. Airway tissue was obtained by blunt dissection and RNA was isolated for miRNA profiling. On the basis of the results obtained, animals were subsequently treated with either an antagomir to miR-126 (ant-miR-126) or a scrambled control antagomir once weekly during the 6 weeks of chronic challenge, and the effects on airway inflammation and remodelling were assessed using established morphometric techniques. Results: Compared to naïve mice, there was selective upregulation of a modest number of miRNAs, notably miR-126, in the airway wall tissue of chronically challenged animals. The relative increase was maximal after 2 weeks of inhalational challenge and subsequently declined to baseline levels. Compared to treatment with the scrambled control, ant-miR-126 significantly reduced recruitment of intraepithelial eosinophils, but had no effect on the chronic inflammatory response, or on changes of airway remodelling. Conclusions: In this model of chronic asthma, there was an initial increase in expression of a small number of miRNAs in the airway wall, notably miR-126. However, this later declined to baseline levels, suggesting that sustained changes in miRNA may not be essential for perpetuation of chronic asthma. Moreover, inhibition of miR-126 by administration of an antagomir suppressed eosinophil recruitment into the airways but had no effect on chronic inflammation in the airway wall, or on changes of remodelling, suggesting that multiple miRNAs are likely to regulate the development of these lesions

Effects of glucocorticoid and phosphodiesterase-4 inhibitor therapy in a mouse model of chronic asthma

Asthma is a chronic inflammatory disease of the airways. Using a murine model which replicates many characteristic features of human asthma, this study evaluated the effects of treatment with anti-inflammatory drugs on the lesions of chronic asthma, and investigated potential underlying molecular mechanisms. Treatment with dexamethasone, a glucocorticoid, was compared with roflumilast, a novel phosphodiesterase-4 (PDE4) inhibitor. BALB/c mice sensitised to ovalbumin were challenged with a low mass concentration of aerosolised antigen for 30 min/day, 3 days/week for 6 weeks. In weeks 5 and 6, groups of animals were treated with either dexamethasone or roflumilast. Assessment included changes in acute-on-chronic inflammation, structural remodelling of the airways and airway hyper-responsiveness to a bronchoconstrictor stimulus. These were correlated with the expression of pro-inflammatory cytokines and growth factors. Compared to vehicle-treated control animals, dexamethasone- and roflumilast-treated mice exhibited reduced accumulation of intra-epithelial eosinophils and chronic inflammatory cells, including CD3+ T-lymphocytes in the airways. Similarly, both drugs inhibited subepithelial fibrosis and airway epithelial thickening, although only dexamethasone inhibited goblet cell hyperplasia/metaplasia. Airway hyper-reactivity was not diminished by either drug. Both treatments suppressed production of Th2 cytokines by ovalbumin-restimulated peribronchial lymph node cells. In selectively dissected airway tissue from vehicletreated animals, increased expression of mRNA for several pro-inflammatory cytokines (TNF-&#945;, GM-CSF, IL-6) and cytokines characteristic of Th1 (IFN-&#947;), Th2 (IL-5, IL-13)and Th17 (IL-17A) cells was demonstrated using real-time PCR. Enhanced expression of growth factors (TGF-&#946;1 and FGF-2) was also demonstrated in airway epithelium isolated by laser capture microdissection. Interestingly, whereas treatment with dexamethasone significantly inhibited expression of mRNA for all of the inflammationrelated cytokines examined, roflumilast inhibited only IL-17A, TNF-&#945;, GM-CSF and IL-6. Both drugs inhibited mRNA expression of growth factors by epithelial cells. Because roflumilast was as effective as dexamethasone in suppressing inflammation and most changes of remodelling, the selective suppression of IL-17A, TNF-&#945;, GM-CSF and IL-6 suggests that these mediators, or the cells that produce them, may have critical roles in pathogenesis. Furthermore, they may be particularly appropriate therapeutic targets in chronic asthma

Resolvin E1 promotes resolution of inflammation in a mouse model of an acute exacerbation of allergic asthma. Clinical science

Abstract Endogenous mediators, such as RvE1 (resolvin E1), promote resolution of an inflammatory response and have potential as novel therapeutic agents. In the present study, we investigated the activity of RvE1 in a model of an acute exacerbation of chronic allergic asthma in mice. Animals sensitized to OVA (ovalbumin) received controlled low-level challenge with aerosolized antigen for 4 weeks, followed by a single moderate-level challenge to simulate an allergen-induced exacerbation of asthmatic inflammation. Induction of an exacerbation was associated with rapid recruitment of neutrophils, lymphocytes and eosinophils, together with increased levels of Th2 and pro-inflammatory cytokines. When administered before the final moderate-level challenge, RvE1 had only a modest effect on airway inflammation. To assess its effects when administered after induction of an exacerbation, we first characterized the cellular and molecular events associated with spontaneous resolution of airway inflammation over the following 96 h. Subsequently, we showed that administration of RvE1 at 2 and 8 h after the final challenge accelerated this process significantly. Specifically, RvE1 promoted a decline in the number of inflammatory cells, concentration of cytokines in lavage fluid and expression of mRNA for cytokines by macrophages, confirming its pro-resolution activity. In vitro, RvE1 had no apparent effect on lymphocytes, but suppressed significantly cytokine production by pulmonary macrophages, with evidence of down-regulation of the nuclear translocation of NF-κB (nuclear factor κB) p65 in these cells. The present study provides novel evidence that RvE1 can facilitate resolution of airway inflammation in a clinically relevant model of an acute exacerbation of asthma, possibly via its effects on activated pulmonary macrophages

The 'classical' ovalbumin challenge model of asthma in mice

Ovalbumin challenge models of asthma offer many opportunities for increasing our understanding of the pathogenetic mechanisms underlying this disease, as well as for identifying novel therapeutic targets. There is no single "classical" model, because numerous alternatives exist with respect to the choice of mouse strain, method of sensitisation, route and duration of challenge, and approach to assessing the host response. Moreover, the limitations of these models need to be recognised when attempting to interpret experimental findings. Nevertheless, careful use of well-defined models allows investigators to answer specific questions that are otherwise difficult to address

CD4(+) T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

Asthma is an acute-on-chronic inflammatory disease of the airways, characterized by airflow obstruction and hyper-reactivity of the airways to a variety of stimuli. Chronic asthma is associated with remodeling of the airway wall, which may contribute to hyper-reactivity and fixed airflow obstruction. We used an improved mouse model of chronic asthma to investigate the role of CD4+ T-lymphocytes in airway remodeling and hyper-reactivity. Animals functionally depleted of CD4+ T-lymphocytes by repeated administration of a monoclonal antibody exhibited markedly decreased airway responsiveness. In addition, these mice had greatly diminished subepithelial fibrosis, epithelial thickening, and mucous cell hyperplasia/metaplasia. Chronic inflammation in the airway wall was moderately reduced, with a marked decrease in the accumulation of immunoglobulin- synthesizing plasma cells. However, intraepithelial accumulation of eosinophils was not significantly inhibited and airway epithelial expression of eotaxin was undiminished. This work provides the first experimental evidence that CD4+ T-lymphocytes play a crucial role in the pathogenesis of the lesions of chronic asthma and lends support to the notion that functional inhibition of these cells may be an important therapeutic target

Interferon-gamma as a Possible Target in Chronic Asthma

The role of interferon-γ (IFN-γ) in asthma is controversial. However, this cytokine has been proposed to play a role both acute severe asthma and chronic stable asthma. We have shown that in a chronic low-level challenge model of allergic asthma in mic