https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53713 Wed 28 Feb 2024 16:37:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51290 Wed 28 Feb 2024 16:16:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53765 Wed 28 Feb 2024 15:59:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52054 Wed 27 Sep 2023 15:30:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38300 AntagomiRs are synthetic antagonists of miRNA, which prevent the target mRNA from suppression. Therapeutic approaches that modulate miRNAs have immense potential in the treatment of chronic respiratory disorders. However, the successful delivery of miRNAs/antagomiRs to the lungs remains a major challenge in clinical applications. A range of materials, namely, polymer nanoparticles, lipid nanocapsules and inorganic nanoparticles, has shown promising results for intracellular delivery of miRNA in chronic respiratory disorders. This review discusses the current understanding of miRNA biology, the biological roles of antagomiRs in chronic respiratory disease and the recent advances in the therapeutic utilization of antagomiRs as disease biomarkers. Furthermore our review provides a common platform to debate on the nature of antagomiRs and also addresses the viewpoint on the new generation of delivery systems that target antagomiRs in respiratory diseases.]]> Wed 27 Oct 2021 10:02:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40357 Wed 27 Jul 2022 15:15:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45172 Wed 26 Oct 2022 14:18:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45076 ELN gene expression in tumors from CRC patients and adjacent non-tumor colon tissues and healthy controls from two existing microarray datasets. ELN protein was measured in human normal colon cells and colon cancer epithelial cells and tumor development was assessed in colon epithelial cells cultured in medium with or without ELN peptide on plates coated with ELN recombinant protein. Control plates were coated with PBS only. Results: We found ELN gene expression was increased in tumors from CRC patients compared to adjacent non-tumor tissues and healthy controls. ELN protein was increased in cancer cells compared to normal colon epithelial cells. Transforming growth factor beta (TGF-β) was a key cytokine to induce production of ECM proteins, but it did not induce ELN expression in colon cancer cells. Matrix metalloproteinase 9 (MMP9) gene expression was increased, but that of MMP12 (elastase) did not change between CRC patients and control. Tissue inhibitor of metalloproteinases 3 (TIMP3) gene expression was decreased in colon tissues from CRC patients compared to healthy controls. However, MMP9, MMP12 and TIMP3 proteins were increased in colon cancer cells. ELN recombinant protein increased proliferation and wound healing in colon cancer epithelial cells. This had further increased in cancer cells incubated in plates coated with recombinant ELN coated plate and in culture media containing ELN peptide. A potential mechanism was that ELN induced epithelial mesenchymal transition with increased alpha-smooth muscle actin and vimentin proteins but decreased E-cadherin protein. Tumor necrosis factor alpha (TNF) mRNA was also increased in CRC patients compared to controls. ELN recombinant protein induced further increases in TNF protein in mouse bone marrow derived macrophages after lipopolysaccharide stimulation. Conclusions: These data suggest ELN regulates tumor development and the microenvironment in CRC.]]> Wed 26 Oct 2022 12:30:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45088 Wed 26 Oct 2022 12:23:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47737 Wed 25 Jan 2023 15:07:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47714 Wed 25 Jan 2023 11:52:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55346 Wed 22 May 2024 12:26:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43527 Wed 21 Sep 2022 11:32:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49965 Wed 21 Jun 2023 11:57:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37130 Wed 19 Aug 2020 12:59:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38204 Wed 18 Aug 2021 09:53:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36824 Wed 17 Nov 2021 16:29:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38603 Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2_α) by 53–83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE₂ and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of ll1b, ll6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE₂ in mouse uterine horn and cervix.]]> Wed 17 Nov 2021 15:27:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48369 Fbln1c-deficient (Fbln1c^–/–) mice had reduced pulmonary remodeling/fibrosis and improved lung function after bleomycin challenge. Fbln1c interacted with fibronectin, periostin, and tenascin-C in collagen deposits following bleomycin challenge. In a potentially novel mechanism of fibrosis, Fbln1c bound to latent TGF-β–binding protein 1 (LTBP1) to induce TGF-β activation and mediated downstream Smad3 phosphorylation/signaling. This process increased myofibroblast numbers and collagen deposition. Fbln1c and LTBP1 colocalized in lung tissues from patients with IPF. Thus, Fbln1c may be a novel driver of TGF-β–induced fibrosis involving LTBP1 and may be an upstream therapeutic target.]]> Wed 15 Mar 2023 13:12:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41157 Wed 15 Feb 2023 10:57:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43214 Wed 14 Sep 2022 14:34:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49614 Wed 14 Jun 2023 16:04:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37964 Wed 14 Jul 2021 08:29:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47176 Wed 14 Dec 2022 15:55:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47144 in vitro. LPS was used to stimulate BEAS-2-B cells, causing the generation of nitric oxide (NO) and other reactive oxygen species (ROS) that had led to cellular apoptosis. The levels of NO and ROS were detected by, Griess reagent kit and dichlorodihydrofluorescein diacetate (DCFH-DA) respectively, whereas, cell apoptosis was studied by Annexin V-FITC and PI staining. The findings revealed that rutin-loaded LCNs significantly reduced NO, ROS levels and prevented apoptosis in BEAS-2B cells. The observations and findings provide a mechanistic understanding of the effectiveness of rutin-loaded LCNs in protecting the bronchial cells against airway inflammation, thus possessing a promising therapeutic option for the management of airway diseases.]]> Wed 14 Dec 2022 15:27:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47060 Wed 13 Mar 2024 08:04:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53640 Wed 13 Dec 2023 10:34:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42686 Wed 08 May 2024 12:01:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41553 Wed 08 May 2024 09:45:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49859 Wed 07 Jun 2023 10:25:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40215 Wed 06 Jul 2022 16:26:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44025 1), Compritol® 888 ATO (X₂) and equal ratio of poloxamer 188: sodium taurocholate (% w/w) (X₃) on particle size, zeta potential and entrapment efficiency. The optimised formulation (SLN₈) was found to be spherical in shape with mean particle size 187.9 ± 10.73 nm and zeta potential −47.4 mV. The maximum percentage entrapment of RIF, INH and PYZ in the optimised formulation was found to be 86.40 ± 0.274, 83.84 ± 0.269 and 81.43 ± 0.576, respectively. The in-vitro drug release study demonstrated that the release of drug from SLNs was slow in comparison to marketed formulation and pure ATDs. Cytotoxicity of the ATDs-SLNs was studied on murine macrophage cell line (RAW 264.7) using modified MTT assay demonstrated two folds growth inhibition of M. marinum as compared to standard antitubercular drugs. Overall, the developed SLNs may be considered as a promising anti-mycobacterial nano-drug, providing a new direction to the tuberculosis clinics.]]> Wed 05 Oct 2022 15:25:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48779 Wed 05 Apr 2023 14:30:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52146 Wed 04 Oct 2023 10:20:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38106 Wed 04 Aug 2021 09:52:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49760 Tue 30 May 2023 18:39:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54542 Tue 27 Feb 2024 20:40:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54474 Tue 27 Feb 2024 14:35:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53957 Tue 23 Jan 2024 10:53:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53288 Tue 21 Nov 2023 10:30:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43418 Tue 20 Sep 2022 08:26:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54347 Tue 20 Feb 2024 16:20:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54312 Tue 20 Feb 2024 14:27:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42000 Tue 16 Aug 2022 16:44:41 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41995 Tue 16 Aug 2022 16:37:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46351 n = 115) and Perth (n = 30), Australia. The Newcastle cohort was enriched with people with asthma (n = 37) and COPD (n = 38). Gene expression for ACE2 and other genes potentially associated with SARS-CoV-2 cell entry was assessed by qPCR, and protein expression was confirmed with immunohistochemistry on endobronchial biopsies and cultured AEC. Results: Increased gene expression of ACE2 was associated with older age (P = 0.03) and male sex (P = 0.03), but not with pack-years smoked. When we compared gene expression between adults with asthma, COPD and healthy controls, mean ACE2 expression was lower in asthma patients (P = 0.01). Gene expression of furin, a protease that facilitates viral endocytosis, was also lower in patients with asthma (P = 0.02), while ADAM-17, a disintegrin that cleaves ACE2 from the surface, was increased (P = 0.02). ACE2 protein expression was also reduced in endobronchial biopsies from asthma patients. Conclusion: Increased ACE2 expression occurs in older people and males. Asthma patients have reduced expression. Altered ACE2 expression in the lower airway may be an important factor in virus tropism and may in part explain susceptibility factors and why asthma patients are not over-represented in those with COVID-19 complications.]]> Tue 15 Nov 2022 15:15:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46337 P = .01), emergency visit (RR = 8.61, P = .03), and hospitalization (RR = 12.94, P < .01). Results of the cluster analysis were successfully validated in an independent PGA population classified using decision tree analysis. Although PGA can transform into or develop from other phenotypes, 70% were stable over time. Conclusions: Among 3 identified PGA clusters, cluster 3 had a higher risk of severe exacerbation. PGA heterogeneity indicates the requirement of novel targeted interventions.]]> Tue 15 Nov 2022 15:03:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41168 Tue 15 Aug 2023 14:44:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50999 Tue 15 Aug 2023 11:52:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48325 Tue 14 Mar 2023 16:33:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47013 Tue 13 Dec 2022 11:48:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47003 Tue 13 Dec 2022 10:59:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43823 Tue 04 Oct 2022 11:04:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39910 Thu 30 Jun 2022 12:44:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40658 Thu 28 Jul 2022 12:42:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41194 Thu 28 Jul 2022 11:12:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41158 Thu 28 Jul 2022 09:27:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45342 Thu 27 Oct 2022 15:17:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45028 Zfp36 gene is an anti‐inflammatory protein that induces mRNA decay, especially of transcripts encoding inflammatory cytokines, including those implicated in COPD. Methods: Here, we identify a novel protective role for TTP in CS‐induced experimental COPD using Zfp36^aa/aa mice, a genetically modified mouse strain in which endogenous TTP cannot be phosphorylated, rendering it constitutively active as an mRNA‐destabilising factor. TTP wild‐type (Zfp36^+/+) and Zfp36^aa/aa active C57BL/6J mice were exposed to CS for four days or eight weeks, and the impact on acute inflammatory responses or chronic features of COPD, respectively, was assessed. Results: After four days of CS exposure, Zfp36^aa/aa mice had reduced numbers of airway neutrophils and lymphocytes and mRNA expression levels of cytokines compared to wild‐type controls. After eight weeks, Zfp36^aa/aa mice had reduced pulmonary inflammation, airway remodelling and emphysema‐like alveolar enlargement, and lung function was improved. We then used pharmacological treatments in vivo (protein phosphatase 2A activator, AAL_(S), and the proteasome inhibitor, bortezomib) to promote the activation and stabilisation of TTP and show that hallmark features of CS‐induced experimental COPD were ameliorated. Conclusion: Collectively, our study provides the first evidence for the therapeutic potential of inducing TTP as a treatment for COPD.]]> Thu 27 Oct 2022 09:28:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48574 Thu 24 Aug 2023 15:19:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51168 Thu 24 Aug 2023 14:09:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51390 Thu 23 Nov 2023 14:31:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53391 Thu 23 Nov 2023 13:37:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38252 Thu 19 Aug 2021 11:04:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38949 Thu 17 Mar 2022 08:49:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47210 Thu 15 Dec 2022 17:18:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39902 Thu 14 Jul 2022 12:11:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36636 Thu 09 Dec 2021 11:03:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49088 Thu 04 May 2023 13:43:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46730 Thu 01 Dec 2022 10:28:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38312 Mon 29 Jan 2024 18:01:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38383 Mon 29 Jan 2024 17:45:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48673 Mon 27 Mar 2023 14:11:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49577 Mon 22 May 2023 10:51:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42355 Mon 22 Aug 2022 14:01:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51768 Mon 18 Sep 2023 14:30:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51767 Mon 18 Sep 2023 14:30:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41886 PXS-5120A (12k), a potent, irreversible inhibitor that is >300-fold selective for LOXL2 over LOX. PXS-5120A also shows potent inhibition of LOXL3, an emerging therapeutic target for lung fibrosis. Key to the development of this compound was the utilization of a compound oxidation assay. PXS-5120A was optimized to show negligible substrate activity in vitro for related amine oxidase family members, leading to metabolic stability. PXS-5120A, in a pro-drug form (PXS-5129A, 12o), displayed anti-fibrotic activity in models of liver and lung fibrosis, thus confirming LOXL2 as an important target in diseases where collagen cross-linking is implicated.]]> Mon 15 Aug 2022 15:37:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46962 Il22^−/−) mice. CS-induced airway remodelling and emphysema-like alveolar enlargement did not occur in Il22^−/− mice. Il22^−/− mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance. These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.]]> Mon 12 Dec 2022 14:27:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44177 Mon 10 Oct 2022 10:20:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55080 Mon 08 Apr 2024 14:10:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50075 Fri 30 Jun 2023 12:02:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48427 Fri 26 Apr 2024 13:31:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54960 Fri 22 Mar 2024 15:34:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40012 Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa)to induce infection in both the respiratory and gastroin-testinal (GI) tracts. However, the importance and mechanism of HIF-1αin augmenting PAFR-dependent bacterial infections in COPD are poorly understood. Here, we review the evidence for the roles of local tissue hypoxia-induced inflammation, HIF-1α and PAFR in facilitating bacterial infections in COPD. Blocking PAFR may provide a novel antimicrobial approach to manage bacterial infections in COPD.]]> Fri 22 Jul 2022 13:06:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53870 Fri 19 Jan 2024 12:39:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46346 via NF-κB, eicosanoid biosynthesis via the lipoxygenase pathway and IL-2 biosynthesis (all P<.01). Sputum macrophage number and the ES for most macrophage signatures were higher in the TAC3 group compared to TAC1 and TAC2 asthmatics. However, a high enrichment was found in TAC1 for 3 modules showing inflammatory pathways linked to Toll-like and TNF receptor activation and arachidonic acid metabolism (P<.001) and in TAC2 for the inflammasome and interferon signalling pathways (P<.001). Data were validated in the ADEPT cohort. Module analysis provides additional information compared to conventional M1 and M2 classification. TR-Mφ were enriched in TAC3 and associated with mitochondrial function. Conclusions: Macrophage activation is attenuated in severe granulocytic asthma highlighting defective innate immunity except for specific subsets characterized by distinct inflammatory pathways.]]> Fri 18 Nov 2022 10:08:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46350 Fri 18 Nov 2022 10:03:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47212 Fri 16 Dec 2022 10:09:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40169 in vitro model of the pulmonary epithelial-endothelial barrier and novel murine models to investigate the role of glycemic variability in influenza severity. In vitro, a history of glycemic variability significantly increased influenza-driven cell death and destruction of the epithelial-endothelial barrier. In vivo, influenza virus-infected mice with a history of glycemic variability lost significantly more body weight than mice with constant blood glucose levels. This increased disease severity was associated with markers of oxidative stress and hyperinflammation both in vitr and in vivo. Together, these results provide the first indication that glycemic variability may help drive the increased risk of severe influenza in people with diabetes mellitus.]]> Fri 15 Jul 2022 10:39:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40156 Fri 15 Jul 2022 09:51:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38589 Fri 12 Nov 2021 15:59:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49363 Fri 12 May 2023 12:42:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41804 Fri 12 Aug 2022 12:31:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41789 Fri 12 Aug 2022 12:17:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41761 Fri 12 Aug 2022 11:42:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38952 Haemophilus influenzae (NTHi), using immunofluorescence microscopy. In addition, expression of a known receptor of NTHi, platelet-activating factor receptor (PAFR), and two pro-inflammatory cytokines, interleukin 6 (IL-6) and interleukin-8 (IL-8), were determined using quantitative polymerase chain reaction. We observed a dose-dependent increase in NTHi adhesion to human bronchial epithelial cells following exposure to cow dung but not wood smoke extracts. Pre-treatment with PAFR antagonists, WEB-2086 and its analogue, C17, decreased adherence by NTHi to airway epithelial cells exposed to cow dung smoke. Both cow dung and wood smoke-induced expression of PAFR, as well as of IL-6 and IL-8, which was inhibited by WEB-2086 and C17. In conclusion, biomass smoke from combustion of cow dung and wood-induced expression of PAFR and airway inflammatory markers in human bronchial epithelial cells. Cow dung exposure, but not wood smoke exposure, mediated a measurable increase in NTHi adhesion to airway epithelial cells that was inhibited by PAFR antagonists. This work highlights the potential of PAFR as a therapeutic target for reducing the impact of hazardous biomass smoke exposure on respiratory health.]]> Fri 11 Mar 2022 14:48:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53577 Fri 08 Dec 2023 15:38:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55056 Fri 05 Apr 2024 14:28:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45706 Fri 04 Nov 2022 08:55:56 AEDT ]]>