https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53765 Wed 28 Feb 2024 15:59:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49984 Wed 28 Feb 2024 15:55:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51883 Wed 28 Feb 2024 15:48:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51366 Wed 28 Feb 2024 15:46:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54338 Wed 28 Feb 2024 15:14:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11267 Wed 24 Jul 2013 22:28:44 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21992 Bacillus species were identified compared with healthy controls. PCR analyses revealed increased rates of detection of potentially pathogenic bacteria with Haemophilus influenzae detection associated with higher sputum levels of NE and IL-1β, while Streptococcus pneumoniae was more common in male ex-smokers with emphysema and a deficit in diffusion capacity. Conclusion: Non-pathogenic and pathogenic bacteria were altered in the sputum of patients with COPD. These observations highlight the potential to identify treatment and management strategies that both target specific bacterial pathogens and restore the microbial balance, which may lead to reductions in inflammation and subsequent improvements in lung health.]]> Wed 17 Nov 2021 16:31:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24377 1.5 fold in subjects with asthma, whereas, in healthy controls, only 14 entities were differentially expressed. Of the 168 genes that were changed in asthma, several biological processes were overrepresented, with 25 genes involved in "immune system processes". qPCR confirmed that S100P, S100A16, MAL and MUC1 were significantly increased in the asthma group post-meal. We also observed a strong correlation and a moderate correlation between the change in NLRP12 and S100A16 gene expression at 4 h compared to baseline, and the change in total and saturated non-esterified plasma fatty acid levels at 2 h compared to baseline. In summary, our data identifies differences in inflammatory gene expression that may contribute to increased airway neutrophilia following a high fat meal in subjects with asthma and may provide useful therapeutic targets for immunomodulation. This may be particularly relevant to obese asthmatics, who are habitually consuming diets with a high fat content.]]> Wed 17 Nov 2021 16:29:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25338 s = 0.398, P = 0.015) and (r_s = 0.455, P = 0.005) respectively), with 1.7% greater absolute weight loss at week 10 corresponding to each one unit reduction in the asthma-related quality of life score at baseline. Furthermore, a lower baseline forced expiratory volume in 1 s/forced vital capacity correlated with greater weight loss (r_s = 0.398, P = 0.015). Male sex was associated with a 3.6 kg greater weight loss (P = 0.087). Reducing emotional eating during the programme was associated with greater weight loss in women (r_s = 0.576, P = 0.010). Conclusions This study demonstrates that individuals with more severe asthma at baseline are more successful in achieving weight loss, which could be a consequence of greater motivation and could be used as a motivational tool within the clinical setting. Gender tailoring of weight loss programmes may be useful to enhance weight loss success. Future studies are urgently needed to establish predictors of long-term weight loss maintenance in those with asthma. See Editorial, page 179 This study is the first to demonstrate that more severe asthma at baseline, male sex, and improvements in eating behaviours during weight loss are associated with greater weight loss success in overweight and obese adults with asthma. Our findings may inform the development of asthma-specific weight management guidelines.]]> Wed 11 Apr 2018 16:17:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22587 0.75, n=7), and healthy controls (HC) (n=9) were stimulated with bacterial (LPS (1 g/mL), fMLF (100 nM)), and viral (imiquimod (3 g/mL), R848 (1.5 g/mL), and poly I:C (10 g/mL)) surrogates or live rhinovirus (RV) 16 (MOI1). Cell-free supernatant was collected after 1 h for neutrophil elastase (NE) and matrix metalloproteinase- (MMP-) 9 measurements or after 24 h for CXCL8 release. Results: Constitutive NE was enhanced in AGood neutrophils compared to HC. fMLF stimulated neutrophils from ASubopt but not AGood produced 50% of HC levels. fMLF induced MMP-9 was impaired in ASubopt and AGood compared to HC. fMLF stimulated CXCL8 but not MMP-9 was positively correlated with FEV1 and FEV1/FVC. ASubopt and AGood responded similarly to other stimuli. Conclusions: Circulating neutrophils are different in asthma; however, this is likely to be related to airflow limitation rather than asthma control.]]> Wed 11 Apr 2018 14:23:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10027 Wed 11 Apr 2018 14:21:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6954 Wed 11 Apr 2018 13:48:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15377 Wed 11 Apr 2018 13:30:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16773 Wed 11 Apr 2018 13:24:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25075 Wed 11 Apr 2018 12:27:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27569 Wed 11 Apr 2018 11:56:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13797 Wed 11 Apr 2018 11:18:00 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7661 Wed 11 Apr 2018 10:52:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17958 Wed 11 Apr 2018 09:41:07 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14143 Wed 11 Apr 2018 09:25:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32663 Wed 10 Nov 2021 15:04:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14664 Wed 04 Sep 2019 11:10:47 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21107 Wed 04 Sep 2019 10:31:12 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44806 Wed 01 May 2024 12:05:04 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21583 Tue 26 Jun 2018 11:28:28 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54370 Tue 20 Feb 2024 19:58:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38233 Tue 17 Aug 2021 08:35:47 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54571 Tue 14 May 2024 14:15:56 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47084 Tue 13 Dec 2022 16:35:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51598 Tue 12 Sep 2023 12:25:08 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53621 Tue 12 Dec 2023 15:19:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38580 Tue 09 Nov 2021 15:45:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38811 Tue 08 Feb 2022 14:30:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51437 Tue 05 Sep 2023 17:56:30 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39063 Tue 03 May 2022 11:38:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36424 61% or >162x10⁴ cells per mL sputum neutrophils) were randomised to receive either azithromycin or placebo for 12 weeks. Sputum and blood were obtained before and after 12 weeks of treatment. Gene expression was defined using microarrays. Networks were analysed using the Search Tool for the Retrieval of Interacting Gene database. In sputum, 403 genes were differentially expressed following azithromycin treatment (171 downregulated and 232 upregulated), and three following placebo treatment (one downregulated and two upregulated) compared to baseline (adjusted p<0.05 by paired t-test, fold-change >1.5). In blood, 138 genes were differentially expressed with azithromycin (121 downregulated and 17 upregulated), and zero with placebo compared to baseline (adjusted p<0.05 by paired t-test, fold-change >1.3). Network analysis revealed one key network in both sputum (14 genes) and blood (46 genes), involving interferon-stimulated genes, human leukocyte antigens and genes regulating T-cell responses. Long-term, low-dose azithromycin is associated with downregulation of genes regulating antigen presentation, interferon and T-cell responses, and numerous inflammatory pathways in the airways and blood of neutrophilic COPD patients.]]> Thu 30 Apr 2020 12:50:04 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54560 Thu 29 Feb 2024 10:27:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36051 Thu 28 Oct 2021 13:04:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26123 Thu 28 Oct 2021 13:04:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35593 Thu 28 Oct 2021 13:03:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31397 IL1R1, IL1R2, and IL1RN), and signaling molecules (IRAK2, IRAK3, and PELI1), were measured in sputum using real-time quantitative polymerase chain reaction. Mediators were compared between the frequent (≥2 exacerbations in the 12 months) and infrequent exacerbators, and the predictive relationships investigated using receiver operating characteristic curves and area under the curve (AUC) values. Results: Of the 95 participants, 89 completed the exacerbation follow-up, where 30 participants (n=22 COPD, n=8 asthma) had two or more exacerbations. At the baseline visit, expressions of IRAK2, IRAK3, PELI1, and IL1R1 were elevated in participants with frequent exacerbations of both asthma and COPD combined and separately. In the combined population, sputum gene expression of IRAK3 (AUC=75.4%; P<0.001) was the best predictor of future frequent exacerbations, followed by IL1R1 (AUC=72.8%; P<0.001), PELI1 (AUC=71.2%; P<0.001), and IRAK2 (AUC=68.6; P=0.004). High IL-1 pathway gene expression was associated with frequent prior year exacerbations and correlated with the number and severity of exacerbations. Conclusion: The upregulation of IL-1 pathway mediators is associated with frequent exacerbations of obstructive airway disease. Further studies should investigate these mediators as both potential diagnostic biomarkers predicting at-risk patients and novel treatment targets]]> Thu 28 Oct 2021 13:03:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32992 Haemophilus influenzae (NTHi), and expression of genes involved in various inflammatory pathways was assessed. Result: NTHi induced production of large amounts of IL-1ß, IL-6, and IL-8 in adult-control BAL cells, ho wever BAL cells from PBB airways appeared refractory to NTHi stimulation. BAL cells from PBB and bronchiectasis showed differential expression of several genes relative to control cells, including CCL20, MARCO, CCL24, IL-10, PPAR-¿, CD200R, TREM2, RelB. Expression of genes involved in resolution of inflammation and anti-inflammation response, such as CD200R and IL-10, was associated with the number of pathogenic bacteria found in the airways. Conclusion: In summary, we have shown that the expression of genes related to macrophage function and resolution of inflammation are similar in PBB and bronchiectasis. Lung immune cell dysfunction in PBB and bronchiectasis may contribute to poor bacterial clearance and prolonged resolution of inflammation.]]> Thu 28 Oct 2021 13:03:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24324 Tropheryma whipplei and Haemophilus influenzae in sputum. Adults with neutrophilic asthma had reduced bacterial diversity and species richness. Tropheryma was identified and confirmed with real-time PCR in 12 (40%) participants. Haemophilus occurred most often in a group of younger atopic males with an increased proportion of neutrophils. PCR confirmed the presence of H. influenzae in 35 (76%) participants with poorly controlled asthma. There are phenotype-specific alterations to the airway microbiome in asthma. Reduced bacterial diversity combined with a high prevalence of H. influenzae was observed in neutrophilic asthma, whereas eosinophilic asthma had abundant T. whipplei.]]> Thu 28 Oct 2021 13:02:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40658 Thu 28 Jul 2022 12:42:40 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45375 Thu 27 Oct 2022 16:54:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46415 Thu 24 Nov 2022 13:56:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48967 Thu 20 Apr 2023 10:09:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38607 Thu 18 Nov 2021 10:35:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46923 Thu 08 Dec 2022 09:09:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4601 Sat 24 Mar 2018 10:13:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7994 Sat 24 Mar 2018 08:42:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8465 Sat 24 Mar 2018 08:42:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8406 Sat 24 Mar 2018 08:40:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8459 Sat 24 Mar 2018 08:38:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7452 Sat 24 Mar 2018 08:38:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8668 Sat 24 Mar 2018 08:38:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8664 Sat 24 Mar 2018 08:38:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7529 Sat 24 Mar 2018 08:38:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1310 0.05). Corticotropin-releasing hormone (CRH), a potent vasodilator that acts via the nitric oxide pathway, caused a dose-dependent vasodilatory response in all placentae in vitro. However, CRH-induced dilation was significantly reduced in moderate and severe asthmatics (ANOVA, p < 0.05). Vasoconstrictor responses to potassium chloride and prostaglandin F2alpha were reduced in placentae from moderate and severe asthmatic women (ANOVA, p < 0.05). These studies demonstrate significant differences in placental vascular function in pregnancies complicated by asthma, which may relate directly to the asthma or be a consequence of the associated glucocorticoid treatment. These changes in vascular function in asthmatic pregnancies may contribute to the low-birthweight outcome observed in this condition.]]> Sat 24 Mar 2018 08:32:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1274 2.5%) was 45% in the wheeze group, which was significantly higher than the control group (9.35%, p = 0.04). Eosinophilic bronchitis was present in two children with cough (20%) and two with chest colds (15%, p > 0.05 versus control). In these groups, eosinophilic bronchitis was not associated with airway hyperresponsiveness (AHR) to hypertonic saline (p > 0.05). Children with cough and chest colds reported greater exposure to environmental tobacco smoke. In conclusion, this community-based survey of children with chronic respiratory symptoms has shown that wheeze is a good discriminator for the presence of eosinophilic bronchitis, and that persistent cough and recurrent chest colds without wheeze should not be considered a variant of asthma. Eosinophilic bronchitis did occur in a significant minority of these "variant asthma" syndromes.]]> Sat 24 Mar 2018 08:32:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1373 Sat 24 Mar 2018 08:28:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14776 Sat 24 Mar 2018 08:26:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15289 Sat 24 Mar 2018 08:21:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15430 Sat 24 Mar 2018 08:20:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11184 Sat 24 Mar 2018 08:12:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11323 Sat 24 Mar 2018 08:12:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18281 Sat 24 Mar 2018 08:04:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16925 Sat 24 Mar 2018 08:00:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21800 Haemophilus influenzae is one of the most commonly isolated bacteria. The relationship between chronic airway colonisation and the development of steroid-resistant neutrophilic asthma is unclear. Objectives: To investigate the relationship between H influenzae respiratory infection and neutrophilic asthma using mouse models of infection and ovalbumin (OVA)-induced allergic airways disease. Methods: BALB/c mice were intratracheally infected with H influenzae (day 10), intraperitoneally sensitised (day 0) and intranasally challenged (day 12–15) with OVA. Treatment groups were administered dexamethasone intranasally during OVA challenge. Infection, allergic airways disease, steroid sensitivity and immune responses were assessed (days 11, 16 and 21). Results: The combination of H influenzae infection and allergic airways disease resulted in chronic lung infection that was detected on days 11, 16 and 21 (21, 26 and 31 days after infection). Neutrophilic allergic airways disease and T helper 17 cell development were induced, which did not require active infection. Importantly, all features of neutrophilic allergic airways disease were steroid resistant. Toll-like receptor 4 expression and activation of phagocytes was reduced, but most significantly the influx and/or development of phagocytosing neutrophils and macrophages into the airways was inhibited. Conclusions: The combination of infection and allergic airways disease promotes bacterial persistence, leading to the development of a phenotype similar to steroid-resistant neutrophilic asthma and which may result from dysfunction in innate immune cells. This indicates that targeting bacterial infection in steroid-resistant asthma may have therapeutic benefit.]]> Sat 24 Mar 2018 07:59:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18331 Sat 24 Mar 2018 07:52:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21345 n = 10), and patients with NEA (n = 22) or eosinophilic asthma (EA) (n = 15) using flow cytometry. Results: Granzyme B expression and the ratio of granzyme B to PI-9 positive cells were highest in those with NEA for both CD3+ and CD4+ T cells. The expression of granzyme B was not statistically different between patients with NEA and EA; however, the ratio of granzyme B to PI-9 positive cells for CD3+ T cells was significantly higher in those with NEA compared with EA. Conclusions: Induced sputum provides a non-invasive tool for investigating T cell cytotoxic mediators in the various asthma subtypes. Granzyme B expression is increased in NEA and the contribution of granzyme B to chronic inflammation requires further study.]]> Sat 24 Mar 2018 07:51:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18790 Sat 24 Mar 2018 07:51:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28283 Sat 24 Mar 2018 07:41:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29058 Sat 24 Mar 2018 07:37:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28982 Sat 24 Mar 2018 07:29:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4796 Sat 24 Mar 2018 07:20:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4797 Sat 24 Mar 2018 07:20:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4838 Sat 24 Mar 2018 07:18:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4857 Sat 24 Mar 2018 07:18:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22281 Sat 24 Mar 2018 07:17:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22677 Sat 24 Mar 2018 07:12:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22106 Streptococcus pneumoniae induces Tregs that have potential to be harnessed therapeutically for asthma. In this study, mouse models of AAD were used to identify the S. pneumoniae components that have suppressive properties, and the mechanisms underlying suppression were investigated. We tested the suppressive capacity of type-3-polysaccharide (T3P), isolated cell walls, pneumolysoid (Ply) and CpG. When coadministered, T3P + Ply suppressed the development of: eosinophilic inflammation, Th2 cytokine release, mucus hypersecretion, and AHR. Importantly, T3P + Ply also attenuated features of AAD when administered during established disease. We show that NKT cells contributed to the development of AAD and also were suppressed by T3P + Ply treatment. Furthermore, adoptive transfer of NKT cells induced AHR, which also could be reversed by T3P + Ply. T3P + Ply-induced Tregs were essential for the suppression of NKT cells and AAD, which was demonstrated by Treg depletion. Collectively, our results show that the S. pneumoniae components T3P + Ply suppress AAD through the induction of Tregs that blocked the activity of NKT cells. These data suggest that S. pneumoniae components may have potential as a therapeutic strategy for the suppression of allergic asthma through the induction of Tregs and suppression of NKT cells.]]> Sat 24 Mar 2018 07:10:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54592 Sat 02 Mar 2024 11:19:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37810 Mon 31 Jan 2022 15:14:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38984 9/L and FENO ≤29 ppb. Exacerbations requiring medical intervention were recorded. Results: Among 220 non-smokers (n = 109 control, n = 111 FENO), 1006 treatment decisions were made, with significant group differences after the first and second algorithm applications. 53% of women had NEA. Treatment was better targeted to phenotype in the FENO group: ICS use increased in eosinophilic asthma (EA, 48–86%), while ICS/LABA increased in NEA (11–30%). Fewer women in the FENO group had exacerbations during pregnancy in NEA only (18.9% FENO vs 44% control, P = 0.006). Conclusion: The FENO algorithm was more effective in treating NEA, resulting in reduced exacerbations, compared to a symptom control algorithm. This was not the result of ICS overtreatment, since the benefits occurred at a lower median daily ICS dose. Two applications of the FENO-guided algorithm, one month apart, were sufficient to achieve beneficial effects in terms of asthma exacerbations, among pregnant women with asthma.]]> Mon 29 Jan 2024 17:52:03 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38401 Mon 29 Jan 2024 17:48:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32658 Mon 23 Sep 2019 11:23:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46274 Mon 14 Nov 2022 15:28:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46221 Mon 14 Nov 2022 12:04:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52317 Mon 09 Oct 2023 10:23:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36441 Mon 04 May 2020 13:05:04 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34249 Fri 22 Feb 2019 16:55:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52682 Fri 20 Oct 2023 09:44:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37978 Fri 16 Jul 2021 18:14:37 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49414 Fri 12 May 2023 15:02:09 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22673 Fri 11 Jun 2021 13:31:32 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38377 Fri 10 Sep 2021 12:38:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48167 Fri 10 Mar 2023 18:24:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51535 Fri 08 Sep 2023 12:31:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55056 Fri 05 Apr 2024 14:28:53 AEDT ]]>