https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51290 Wed 28 Feb 2024 16:16:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47729 Wed 25 Jan 2023 14:25:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47714 Wed 25 Jan 2023 11:52:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32527 Wed 17 Nov 2021 16:31:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36824 Wed 17 Nov 2021 16:29:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30281 Fbln1c protected against CS-induced airway fibrosis and emphysema-like alveolar enlargement. In experimental COPD, this occurred through disrupted collagen organization and interactions with fibronectin, periostin, and tenascin-c. Genetic inhibition of Fbln1c also reduced levels of pulmonary inflammatory cells and proinflammatory cytokines/chemokines (TNF-a, IL-33, and CXCL1) in experimental COPD. Fbln1c⌿ mice also had reduced airway remodeling in experimental chronic asthma and pulmonary fibrosis. Our data show that Fbln1c may be a therapeutic target in chronic respiratory diseases.]]> Wed 11 Apr 2018 13:33:47 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33415 Wed 10 Nov 2021 15:04:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30796 60 years), whereas neutrophilic bronchitis (NB) was defined as high total cell count (=5.1×10 6 cells/mL) plus an increased age-corrected neutrophil proportion. The optimal cut-off for sputum colour to predict neutrophilic inflammation and NB was determined using receiver operator characteristic curve analysis. Results: A sputum colour score of =3 represented and predicted neutrophilic inflammation with modest accuracy (area under the curve (AUC)=0.64; p < 0.001, specificity=78.4%, sensitivity=49.2%). Participants with a sputum colour score of =3 had significantly (p < 0.05) higher CXCL-8, total cells and neutrophil number and proportion. Sputum colour score was also positively correlated with these factors. Sputum colour score =3 predicted NB with reasonably good accuracy (AUC=0.79, p < 0.001, specificity=79.3%, sensitivity=70.7%). Conclusions: Visual gradation of sputum colour in asthma relates to high total cell count and neutrophilic inflammation. Assessment of sputum colour can identify adults with asthma who are likely to have NB without the need for spu tum processing and differential cell count, which may facilitate asthma management.]]> Wed 09 Mar 2022 16:04:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52619 Wed 06 Mar 2024 15:31:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34645 0.05). Additionally, VP patients were less likely to have received influenza vaccination. VP patients had a systemic inflammation response involving IL-6, TNF-µ, and MCP-1 which may be due to virus-induced activation of macrophages. There are important opportunities for further investigating AECOPD mechanisms and for the development of better strategies in the management and prevention of virus-related AECOPD.]]> Wed 04 Sep 2019 10:06:43 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26567 TM GX Human Inflammation Kit 2. Results: Following the interventions, clinical characteristics and plasma IL-6 and CRP were unchanged. Sputum neutrophil proportion and absolute count was increased and macrophage proportion decreased by rosuvastatin (P = 0.020 and P = 0.015; respectively). Rosuvastatin increased LTB4R and decreased CXCL10 and AGER gene expression in white blood cells. The addition of lycopene and omega-3 fatty acids decreased LTB4R and increased CXCL10 to basal levels, whilst combined use of interventions increased ALOX15 blood gene expression. Conclusion This study shows that rosuvastatin, omega-3 fatty acids and lycopene have some anti-inflammatory effects systemically, but rosuvastatin may increase airway neutrophils, which would be undesirable in COPD patients, warranting further investigation.]]> Wed 02 Mar 2022 14:27:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52918 Wed 01 Nov 2023 09:31:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52014 Tue 26 Sep 2023 11:42:59 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47626 1), FEV₁, forced vital capacity (FVC), FEV₁/FVC ratio, percent predicted FEV₁ and percent predicted FVC. Multivariable regression models in the general population as well as those with spirometry-defined airflow obstruction were used to assess the relationship between lung function measurements and dietary SFA intake after adjustment for confounders. 11,180 eligible participants were included in this study. Univariate analysis revealed a statistically significant positive association between total SFA intake and lung function outcomes; however, these relationships were attenuated after adjustment for covariates. A secondary analysis of individuals with spirometry-defined airflow obstruction (FEV₁/FVC < 0.7) revealed that a lower intake of SFA was associated with reduced FEV₁ (β = −126.4, p = 0.04 for quartile 1 vs. quartile 4), FVC (β = −165.8. p = 0.01 for quartile 1 vs. quartile 4), and percent predicted FVC (β = −3.3. p = 0.04 for quartile 1 vs. quartile 4), after adjustment for relevant confounders. No associations were observed for the FEV₁/FVC ratio and percent predicted FEV₁. It is possible that characteristics such as food source and fatty acid chain length may influence associations between saturated fatty acid intake and health outcomes.]]> Tue 24 Jan 2023 14:09:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47625 Tue 24 Jan 2023 14:02:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53957 Tue 23 Jan 2024 10:53:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43418 Tue 20 Sep 2022 08:26:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33143 −26) and a 1.4 fold in the severe COPD -related genes (P = 2.3 × 10⁻¹²). There was no significant enrichment of the mice and human smoking-related genes in mild COPD signature. These data suggest that murine smoke models are strongly representative of molecular processes of human smoking but less of COPD.]]> Tue 03 Sep 2019 18:18:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21994 Thu 28 Oct 2021 12:36:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33773 Thu 27 Jan 2022 15:56:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30071 Thu 24 Mar 2022 11:36:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34690 Thu 03 Feb 2022 12:20:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47501 Thu 02 May 2024 15:43:53 AEST ]]> 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:8375 Sat 24 Mar 2018 08:39:49 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:10730 Sat 24 Mar 2018 08:09:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18137 Sat 24 Mar 2018 08:04:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20434 −/− C57BL/6 mouse line. The resulting animals exhibited no obvious developmental abnormality, contained normal numbers of granulated MCs in their tissues, and did not compensate for their loss of the membrane tryptase by increasing their expression of other granule proteases. When Prss31-null MCs were activated with a calcium ionophore or by their high affinity IgE receptors, they degranulated in a pattern similar to that of WT MCs. Prss31-null mice had increased baseline airway reactivity to methacholine but markedly reduced experimental chronic obstructive pulmonary disease and colitis, thereby indicating both beneficial and adverse functional roles for the tryptase. In a cigarette smoke-induced model of chronic obstructive pulmonary disease, WT mice had more pulmonary macrophages, higher histopathology scores, and more fibrosis in their small airways than similarly treated Prss31-null mice. In a dextran sodium sulfate-induced acute colitis model, WT mice lost more weight, had higher histopathology scores, and contained more Cxcl-2 and IL-6 mRNA in their colons than similarly treated Prss31-null mice. The accumulated data raise the possibility that inhibitors of this membrane tryptase may provide additional therapeutic benefit in the treatment of humans with these MC-dependent inflammatory diseases.]]> Sat 24 Mar 2018 08:03:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29214 Sat 24 Mar 2018 07:36:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4818 Sat 24 Mar 2018 07:18:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38585 in vitro airway epithelial infection models using high multiplicity of infection (MOI) and lacking genome-wide, time course analyses have obscured the role of epithelial innate anti-viral immunity in asthma and COPD. To address this, we developed a low MOI rhinovirus model of differentiated primary epithelial cells obtained from healthy, asthma and COPD donors. Using genome-wide gene expression following infection, we demonstrated that gene expression patterns are similar across patient groups, but that the kinetics of induction are delayed in cells obtained from asthma and COPD donors. Rhinovirus-induced innate immune responses were defined by interferons (type-I, II, and III), interferon response factors (IRF₁, IRF₃, and IRF₇), TLR signaling and NF-κB and STAT₁ activation. Induced gene expression was evident at 24 h and peaked at 48 h post-infection in cells from healthy subjects. In contrast, in cells from donors with asthma or COPD induction was maximal at or beyond 72–96 h post-infection. Thus, we propose that propensity for viral exacerbations of asthma and COPD relate to delayed (rather than deficient) expression of epithelial cell innate anti-viral immune genes which in turns leads to a delayed and ultimately more inflammatory host immune response.]]> Mon 29 Jan 2024 18:03:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32170 Mon 23 Sep 2019 13:39:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42308 Camp^-/-) and exogenous cathelicidin prevented ICS-mediated expansion of streptococci within the microbiota and improved bacterial clearance. Suppression of pulmonary immunity by ICS was mediated by augmentation of the protease cathepsin D. Collectively, these data suggest a central role for cathepsin D/cathelicidin in the suppression of antibacterial host defense by ICS in COPD. Therapeutic restoration of cathelicidin to boost antibacterial immunity and beneficially modulate the lung microbiota might be an effective strategy in COPD.]]> Mon 22 Aug 2022 10:35:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55409 Mon 19 Aug 2024 18:01:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51768 Mon 18 Sep 2023 14:30:32 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46232 Mon 14 Nov 2022 12:33:10 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:40195 Mon 08 Aug 2022 13:28:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50075 Fri 30 Jun 2023 12:02:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55396 Fri 24 May 2024 10:54:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33084 Fri 24 Aug 2018 15:43:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54960 Fri 22 Mar 2024 15:34:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49402 Fri 12 May 2023 14:41:04 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:49786 Fri 02 Jun 2023 17:27:41 AEST ]]>