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This article reflects on how patient education tool design can benefit from a co-creation process with patients and key stakeholders involved, using a case study in chronic obstructive pulmonary disease (COPD) care. Unfavourable hospitalisation experiences for COPD patients are often linked to organisational issues and health literacy challenges. This study presents insights from a year-long co-creation practice involving COPD patients, a family member, healthcare practitioners, and hospital managers, aimed at developing patient education tools to enhance health literacy concerning the hospitalisation process. The primary outcome is a set of patient education infographics that can be integrated into digital platforms or printed formats. For such co-creation practice, we found that setting clear creativity expectations and using methods such as user journey maps empower participants. Balancing the power dynamics between patients and healthcare practitioners enables culturally relevant and patient-centred tools. In addition, family members play a crucial role in both co-creation process and care journey, while hospital managers ensure tools align with clinical practices. We also advocate for an ecological perspective towards intervention development, acknowledging diverse needs emerged from the co-creation process. Future research should implement strategies in further individualising infographics to improve their effectiveness.

Choosing the appropriate design process is critical for the effective implementation and long-term sustainment of interventions aimed at addressing public health challenges. To address this need, we proposed a Transition Design model to identify and deliver sustainable solutions for complex healthcare problems. This model generates system-level health-intervention initiatives that can synergistically function, particularly during the development and implementation phases, to enhance healthcare delivery. Drawing from a case study on addressing the challenges of hospitalisations and early discharge for people with acute exacerbations of chronic obstructive pulmonary disease (AECOPD), we reflected on the process and analysed the outcomes. Although further testing for the initiatives is warranted, this study contributes to the evolving discourse in design research on systems solutioning for public-health challenges.

Background: Incorporating co-creation process in the development of interventions may improve the outcome. However, there is a lack of synthesis of co-creation practices in the development of Non-Pharmacological Interventions (NPIs) for Chronic Obstructive Pulmonary Disease (COPD).

Objective: This scoping review aimed to examine the co-creation practice used when developing NPIs for people with COPD.

Methods: The methodology proposed by Arksey and O’Malley for scoping reviews was followed, and it was reported according to the PRISMA-ScR framework. The search included PubMed, Scopus, CINAHL, and Web of Science. Studies reporting on the process and/or analysis of applying co-creation practice in developing NPIs for people with COPD were included.

Results: 13 articles complied with the inclusion criteria. The composition of co-creators was diverse and reported in most of the included studies. Facilitating factors described in the co-creation practices included administrative preparations, diversity of stakeholders, cultural considerations, employment of creative methods, creation of an appreciative environment, and digital assistance. Few creative methods were mentioned or explained in the studies. Challenges around the physical limitations of patients, the absence of key stakeholder opinions, a prolonged process, recruitment, and digital illiteracy of co-creators were listed. Most of the studies did not report implementation considerations as a discussion point in their co-creation workshops.

Conclusion: This review provides suggestions for evidence-based co-creation in COPD care which may improve the quality of care delivered by NPIs.

Background: Incorporating co-creation processes may improve the quality of outcome interventions. However, there is a lack of synthesis of co-creation practices in the development of Non-Pharmacological Interventions (NPIs) for people with Chronic Obstructive Pulmonary Disease (COPD), that could inform future co-creation practice and research for rigorously improving the quality of care.

Objective: This scoping review aimed to examine the co-creation practice used when developing NPIs for people with COPD.

Methods: This review followed Arksey and O'Malley scoping review framework and was reported according to the PRISMA-ScR framework. The search included PubMed, Scopus, CINAHL, and Web of Science Core Collection. Studies reporting on the process and/or analysis of applying co-creation practice in developing NPIs for people with COPD were included.

Results: 13 articles complied with the inclusion criteria. Limited creative methods were reported in the studies. Facilitators described in the co-creation practices included administrative preparations, diversity of stakeholders, cultural considerations, employment of creative methods, creation of an appreciative environment, and digital assistance. Challenges around the physical limitations of patients, the absence of key stakeholder opinions, a prolonged process, recruitment, and digital illiteracy of co-creators were listed. Most of the studies did not report including implementation considerations as a discussion point in their co-creation workshops.

Conclusion: Evidence-based co-creation in COPD care is critical for guiding future practice and improving the quality of care delivered by NPIs. This review provides evidence for improving systematic and reproducible co-creation. Future research should focus on systematically planning, conducting, evaluating, and reporting co-creation practices in COPD care.

BACKGROUND: Ozone concentrations are predicted to increase over the next 50 years due to global warming and the increased release of precursor chemicals. It is therefore urgent that good, reliable biomarkers are available to quantify the toxicity of this pollutant gas at the population level. Such a biomarker would need to be easily performed, reproducible, economically viable, and reflective of ongoing pathological processes occurring within the lung.

METHODOLOGY: We examined whether blood neutrophilia occurred following a controlled ozone challenge and addressed whether this could serve as a biomarker for ozone-induced airway inflammation. Three separate groups of healthy subjects were exposed to ozone (0.2 ppm, 2h) and filtered air (FA) on two separate occasions. Peripheral blood samples were collected and bronchoscopy with biopsy sampling and lavages was performed at 1.5h post exposures in group 1 (n=13), at 6h in group 2 (n=15) and at 18h in group 3 (n=15). Total and differential cell counts were assessed in blood, bronchial tissue and airway lavages.

RESULTS: In peripheral blood, we observed fewer neutrophils 1.5h after ozone compared with the parallel air exposure (-1.1±1.0x10(9) cells/L, p<0.01), at 6h neutrophil numbers were increased compared to FA (+1.2±1.3x10(9) cells/L, p<0.01), and at 18h this response had fully attenuated. Ozone induced a peak in neutrophil numbers at 6h post exposure in all compartments examined, with a positive correlation between the response in blood and bronchial biopsies.

CONCLUSIONS: These data demonstrate a systemic neutrophilia in healthy subjects following an acute ozone exposure, which mirrors the inflammatory response in the lung mucosa and lumen. This relationship suggests that blood neutrophilia could be used as a relatively simple functional biomarker for the effect of ozone on the lung.

Exposure to diesel exhaust at concentrations consistent with roadside levels elicited an acute and active neutrophilic inflammation in the airways of healthy subjects. This response was absent in subjects with asthma, as was evidence supporting a worsening of allergic airway inflammation.

Asthmatics are recognised to be more susceptible than healthy individuals to adverse health effects caused by exposure to the common air pollutant ozone. Ozone has been reported to induce airway neutrophilia in mild asthmatics, but little is known about how it affects the airways of asthmatic subjects on inhaled corticosteroids. We hypothesised that ozone exposure would exacerbate the pre-existent asthmatic airway inflammation despite regular inhaled corticosteroid treatment. Therefore, we exposed subjects with persistent asthma on inhaled corticosteroid therapy to 0.2 ppm ozone or filtered air for 2 h, on 2 separate occasions. Lung function was evaluated before and immediately after exposure, while bronchoscopy was performed 18 h post exposure. Compared to filtered air, ozone exposure increased airway resistance. Ozone significantly enhanced neutrophil numbers and myeloperoxidase levels in airway lavages, and induced a fourfold increase in bronchial mucosal mast cell numbers. The present findings indicate that ozone worsened asthmatic airway inflammation and offer a possible biological explanation for the epidemiological findings of increased need for rescue medication and hospitalisation in asthmatic people following exposure to ambient ozone.

The aim of the study was to characterize ozone-induced antioxidant responses in the human airway, including the resident leukocyte population, bronchial mucosa, and respiratory-tract lining fluids. Fifteen healthy subjects were exposed to 0.2 ppm ozone for 2 h, with bronchial wash, bronchoalveolar lavage, and biopsy sampling performed 6 h postexposure. Nasal lavage was also performed at multiple time points pre- and postexposure to evaluate responses during the actual exposure period. During the ozone challenge significant losses of nasal lining fluid urate and vitamin C were observed, which resolved 6 h postexposure. At this time point, increased numbers of neutrophils and enhanced concentrations of total glutathione, vitamin C, and urate were seen in bronchial airway lavages. In bronchoalveolar lavage, increased concentrations of total glutathione, vitamin C, urate, alpha-tocopherol, and extracellular superoxide dismutase occurred 6 h post ozone. In alveolar leukocytes significant losses of glutathione were observed, whereas ascorbate concentrations in endobronchial mucosal biopsies were elevated after ozone at this time. These data demonstrate that ozone elicits a broad spectrum of airway antioxidant responses, with initial losses of vitamin C and urate followed by a phase of augmentation of low-molecular-weight antioxidant concentrations at the air-lung interface. The temporal association between the increased RTLF glutathione following ozone and the loss of this thiol from macrophages implies a mobilization to the lung surface, despite the absence of a quantitative association. We propose this constitutes an acute protective adaptation to ozone.

Low molecular weight antioxidants within human respiratory tract lining fluids (RTLFs) have been proposed to confer protection against the damaging action of inhaled oxidant gases. There is therefore considerable interest in augmenting the concentrations of these moieties at the air-lung interface to protect against injury to the airway epithelium, the induction of inflammation, and declines in lung function. To determine whether RTLF ascorbate concentrations could be augmented through vitamin C supplementation, 24 healthy subjects with low plasma ascorbate (< 50 microM) were recruited into a double-blinded study. Subjects were divided into two groups, one receiving 60 mg/day of vitamin C for 14 days, the other placebo. On days 8 and 15 of this protocol, plasma, urine, and nasal lavage were obtained for ascorbate determination. After a 7-14-day non-intervention period, subjects previously on placebo received supplements containing 125 mg ascorbate, whilst the group previously on supplements received the placebo compound. This "switching" protocol was repeated three more times utilizing 250, 500, and 1000 mg/day ascorbate dosage regimens. Plasma ascorbate increased incrementally with vitamin C dose, as did its urinary excretion. Despite this, nasal lavage concentrations remained unaltered 24 h after the final supplement at all doses. Closer examination of this issue demonstrated that nasal lavage ascorbate concentrations increased acutely after ingestion of a high dose (1000 mg) supplement, peaking at 2-4 h (p < 0.05) before returning to baseline concentrations 24 h post-supplement. In the absence of a quantitative association between plasma and lavage ascorbate concentrations we contend that this response does not simply reflect ascorbate transudation from the plasma and interstitial space into the lavage medium. We therefore conclude that RTLF ascorbate can be augmented, albeit transiently, by oral vitamin C supplementation, with the transient nature of this response likely reflecting oxidative losses within the RTLF or its sequestration into airway cells.