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Objective: Childhood obesity prevention is critical to reducing the health and economic burden currently experienced by the Australian economy. Systems science has emerged as an approach to manage the complexity of childhood obesity and the ever-changing risk factors, resources and priorities of government and funders. Anecdotally, our experience suggests that inflexibility of traditional research methods, and dense academic terminology created issues with those working in prevention practice. Therefore, this paper provides a refined description of research specific terminology of scale-up, fidelity, adaptation, and context, drawing from community-based systems dynamics and our experience in designing, implementing, and evaluating non-linear, community-led systems approaches to childhood obesity prevention.Design: We acknowledge the importance of using a practice lens, rather than purely a research design lens and provide a narrative on our experience and perspectives on scale-up, fidelity, context and adaptation through a practice lens.Setting: Communities.Participants: Practice-based researcher experience and perspectives.Results: Practice-based researchers highlighted the key finding that community should be placed at the centre of the intervention logic. This allowed communities to self-organise with regards to stakeholder involvement, capacity, boundary identification and co-creation of actions implemented to address childhood obesity will ensure scale up, fidelity, context and adaptation are embedded.Conclusions: We need to measure beyond primary anthropometric outcomes and focus on evaluating more about implementation, process, and sustainability. We need to learn more from practitioners on the ground and use an implementation science lens to further understand how actions work. This is where solutions to sustained childhood obesity prevention will be found. [ABSTRACT FROM AUTHOR]

Introduction: Residents of rural areas internationally typically experience chronic disease risk profiles worse than city dwellers. Poor diet, a key driver of chronic disease, has been associated with unhealthy food environments, and rural areas often experience limited access to healthy, fresh and affordable food. Objective: This study aimed to evaluate the first three years of a health promoting social enterprise café established in a small rural health service. Design: A mixed‐methods evaluation study. Quantitative sales data, surveys and key informant interviews that included both quantitative and qualitative responses. Findings: Three years of sales data were included; 111customer surveys and five key informant interviews were conducted. Food and beverages on displayed and sold consistently met or exceeded the healthy criteria set by policy. Stakeholders supported the traffic light system, the social enterprise model and rated the likelihood of sustainability of the café as high. Discussion: Customers used the 'traffic light' system to inform food choices, placed value on the warmth of the staff and on the welcoming environment created through the social enterprise model. Resources remain tight although all stakeholders are committed to the sustainability of the YarriYak café. Conclusion: The study shows the acceptability, feasibility and sustainability of a health promoting social enterprise café in a rural area. [ABSTRACT FROM AUTHOR]

Coronaviruses are adept at evading host antiviral pathways induced by viral double-stranded RNA, including interferon (IFN) signaling, oligoadenylate synthetase-ribonuclease L (OAS-RNase L), and protein kinase R (PKR). While dysregulated or inadequate IFN responses have been associated with severe coronavirus infection, the extent to which the recently emerged SARS-CoV-2 activates or antagonizes these pathways is relatively unknown. We found that SARS-CoV-2 infects patient-derived nasal epithelial cells, present at the initial site of infection; induced pluripotent stem cell-derived alveolar type 2 cells (iAT2), the major cell type infected in the lung; and cardiomyocytes (iCM), consistent with cardiovascular consequences of COVID- 19 disease. Robust activation of IFN or OAS-RNase L is not observed in these cell types, whereas PKR activation is evident in iAT2 and iCM. In SARS-CoV-2-infected Calu-3 and A549ACE2 lung-derived cell lines, IFN induction remains relatively weak; however, activation of OAS-RNase L and PKR is observed. This is in contrast to Middle East respiratory syndrome (MERS)-CoV, which effectively inhibits IFN signaling and OAS-RNase L and PKR pathways, but is similar to mutant MERS-CoV lacking innate immune antagonists. Remarkably, OASRNase L and PKR are activated in MAVS knockout A549ACE2 cells, demonstrating that SARS-CoV-2 can induce these host antiviral pathways despite minimal IFN production. Moreover, increased replication and cytopathic effect in RNASEL knockout A549ACE2 cells implicates OASRNase L in restricting SARS-CoV-2. Finally, while SARS-CoV-2 fails to antagonize these host defense pathways, which contrasts with other coronaviruses, the IFN signaling response is generally weak. These host-virus interactions may contribute to the unique pathogenesis of SARS-CoV-2. [ABSTRACT FROM AUTHOR]