| 1. |
- An, Qingfan, 1997-, et al.
(författare)
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A scoping review of co-creation practice in the development of non-pharmacological interventions for people with chronic obstructive pulmonary disease : a health CASCADE study
- 2023
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Ingår i: Respiratory Medicine. - : Elsevier. - 0954-6111 .- 1532-3064. ; 211
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Forskningsöversikt (refereegranskat)abstract
- 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.
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| 2. |
- An, Qingfan, 1997-, et al.
(författare)
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A scoping review of co-creation practice in the development of non-pharmacological interventions for people with chronic obstructive pulmonary disease
- 2023
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 62:Suppl. 67
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 3. |
- Behndig, Annelie, et al.
(författare)
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Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.
- 2006
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 27:2, s. 359-365
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Tidskriftsartikel (refereegranskat)abstract
- Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly. A total of 15 volunteers were exposed to DE (100 microg x m(-3) airborne particulate matter with a diameter of <10 microm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status. Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure. In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.
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| 4. |
- Behndig, Annelie, 1963-
(författare)
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Airway antioxidant responses to oxidative air pollution and vitamin supplementation
- 2006
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Air pollutants, such as ozone (O3) and diesel exhaust particles, elicit oxidative stress in the lung. Antioxidants within the respiratory tract lining fluid (RTLF) protect the underlying tissue from oxidative injury. Supplementation with vitamins has been shown to modulate the acute ozone-induced effects, but the mechanisms behind this have not been fully clarified. The aim of this thesis was to investigate the airway responses to diesel exhaust and ozone exposure in healthy humans, with the emphasis on inflammatory and antioxidant responses. Furthermore, to study whether oral supplementation with vitamin C could increase ascorbate concentration in the RTLF and whether vitamin supplementation could modulate the negative effects induced by ozone exposure. Diesel exhaust (100 µg/m3 PM10 for 2h), evaluated 18 hours post exposure (PE), induced a neutrophilic airway inflammation and an increase in bronchoalveolar (BAL) urate and reduced glutathione. During O3 exposure (0.2 ppm for 2h), significant losses of nasal RTLF urate and ascorbate concentrations were observed. Six hours PE, a neutrophilic inflammation was evident in the bronchial wash (BW), together with enhanced concentrations of urate and total glutathione. In the bronchoalveolar lavage (BAL), where vitamin C, urate and glutathione concentrations were augmented, no inflammatory response was seen. In alveolar lavage leukocytes, there was a significant loss of glutathione and cysteine, whereas an increase in ascorbate was found in bronchial tissue samples. Following supplementation with increasing doses of vitamin C (60-1,000 mg/day, for 14 days), evaluated 24 hours after the last dose, ascorbate concentrations were unchanged in the nasal RTLF, despite elevated concentrations in plasma and urine. In contrast, following a single dose of 1g of vitamin C, vitamin C concentrations increased significantly in both plasma and nasal lavage two hours post supplementation, before returning to baseline levels at 24 hours. Notably, dehydroascorbate (DHA) accounted for the largest part of RTLF vitamin C and a number of control experiments were performed to ensure the authenticity of this finding. Healthy O3 responders were exposed to O3 (0.2 ppm for 2 h) and air, following seven days of supplementation with vitamin C and E or placebo. No protective effect on lung function or airway inflammation was observed following supplementation. BW and BAL-DHA were enhanced after O3, with further increases following supplementation. In conclusion, oxidative air pollutants induce airway inflammation, as well as a broad spectrum of antioxidant adaptations, which could ultimately limit the airway inflammatory responses. Oral vitamin supplementation was shown to augment RTLF-vitamin C concentrations, but it did not provide protection from the ozone-induced airway responses following a single insult of ozone. The finding of high concentrations of DHA in the RTLF could indicate that DHA represents an important transport form of vitamin C onto the surface of the lung.
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| 5. |
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| 6. |
- Behndig, Annelie F, et al.
(författare)
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Antioxidant responses to acute ozone challenge in the healthy human airway
- 2009
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Ingår i: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 21:11, s. 933-942
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 7. |
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| 8. |
- Behndig, Annelie F, et al.
(författare)
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Augmentation of respiratory tract lining fluid ascorbate concentrations through supplementation with vitamin C.
- 2009
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Ingår i: Inhalation toxicology. - : Informa UK Limited. - 1091-7691 .- 0895-8378. ; 21:3, s. 250-8
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 9. |
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| 10. |
- Bosson, Jenny A, et al.
(författare)
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Peripheral blood neutrophilia as a biomarker of ozone-induced pulmonary inflammation
- 2013
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 8:12
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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