https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45089 Wed 26 Oct 2022 14:04:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45117 Wed 26 Oct 2022 12:45:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29109 Wed 11 Apr 2018 15:48:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13988 Wed 11 Apr 2018 10:50:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32190 Wed 09 Mar 2022 16:01:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32469 Gossypium hirsutum) fibers. In contrast to wild-type fiber PDs, which opened at 5 to 10 d postanthesis (DPA) and closed only at 15 to 25 DPA, plants with suppressed GhSCP2D expression had reduced sterol contents and closed PDs at 5 through 25 DPA. The GhSCP2D-suppressed fibers exhibited callose deposition at the PDs, likely due to reduced expression of GhPdBG3-2A/D, which encodes a PD-targeting β-1,3-glucanase. Both GhPdBG3-2A/D expression and callose deposition were sensitive to a sterol biosynthesis inhibitor. Moreover, suppressing GhSCP2D upregulated a cohort of SUT and SWEET sucrose transporter genes in fiber cells. Collectively, our results indicate that (1) GhSCP2D is required for GhPdBG3-2A/D expression to degrade callose at the PD, thereby contributing to the establishment of the symplasmic pathway; and (2) blocking the symplasmic pathway by downregulating GhSCP2D activates or increases the expression of SUTs and SWEETs, leading to the switch from symplasmic to apoplasmic pathways.]]> Wed 06 Jun 2018 14:11:15 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45298 6 million deaths globally at the time of writing. COVID-19, instigated by the SARS - coronavirus-2 (SARS-CoV-2), causes unprecedented challenges in all facets of our lives, and never before brought scientists of all fields together to focus on this singular topic. While for the past 50 years research have been heavily focused on viruses themselves, we now understand that the host immune responses are just as important in determining the pathogenesis and outcomes of infection. Research in innate immune mechanisms is crucial in understanding all aspects of host antiviral programmes and the mechanisms underpinning virus-host interactions, which can be translated to the development of effective therapeutic avenues. This review summarizes what is known and what remains to be explored in the innate immune responses to influenza viruses and SARS-CoVs, and virus-host interactions in driving disease pathogenesis. This hopefully will encourage discussions and research on the unanswered questions, new paradigms, and antiviral strategies against these emerging infectious pathogens before the next pandemic occurs.]]> Tue 23 May 2023 08:41:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38714 Tue 18 Jan 2022 15:19:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48327  β-glucosidase > acid phosphatase > FDA hydrolase. Urease activity was generally not affected and showed high stability against heat disturbance. The β-glucosidase activity recovered to the control level by 30 days, while 80% and 90% recovery on average occurred for acid phosphatase and FDA hydrolase, respectively. Long-term As contamination altered soil enzyme functional resistance and resilience to heat disturbance and resulted in three kinds of responses: (i) no apparent alteration (urease); (ii) moderate As contamination increased enzyme heat resistance (β-glucosidase); (iii) the resistance and resilience decreased with increasing As concentration (acid phosphatase and FDA hydrolase). The results demonstrated that different enzyme-catalytic biochemical processes have different functional stabilities under combined As and heat disturbance, and the negative changes in the soil enzyme activity led to losses in soil functions. Our study provides further evidence on the impacts of heavy metal/metalloid on soil enzyme functional stability in response to additional disturbance.]]> Tue 14 Mar 2023 16:47:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54213 Tue 13 Feb 2024 11:50:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45550 Tue 01 Nov 2022 10:56:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45207 Rhodiola wallichiana var. cholaensis (RWC) has the potential to alleviate asthmatic inflammation according to recent studies, but its pharmacological mechanisms remain unclarified. In our study, murine asthmatic phenotypes were established and treated with RWC and/or dexamethasone (DEX). Combined treatment with RWC and DEX could improve spirometry and airway hyperresponsiveness (AHR) in asthmatic phenotypes, alleviate steroid resistance in NEA, and reduce the inflammatory infiltration of the both phenotypes. The combined treatment increased Th1, regulated the imbalance of Th2/Th1, and decreased the related cytokines in EA. As for NEA, the combined treatment reduced Th17 and promoted the accumulation of regulatory T cells (Tregs) in lung. A microbiome study based on 16S rDNA sequencing technique revealed the significantly changed structure of the lower airway microbiota after combined treatment in NEA, with 4 distinct genera and 2 species identified. OPLS-DA models of metabolomics analysis based on UPLC-Q/TOF-MS technique identified 34 differentiated metabolites and 8 perturbed metabolic pathways. A joint multiomics study predicted that the colonized microbiota in airways might be associated with susceptibility of asthma and steroid resistance, which involved systematic and pulmonary metabolic perturbation. In summary, the pharmacological network of RWC included the complicated interaction mechanisms of immune regulation, microbiota change, and metabolic perturbation.]]> Thu 27 Oct 2022 15:07:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51880 Thu 21 Sep 2023 10:25:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12346 Sat 24 Mar 2018 08:18:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23479 Sat 24 Mar 2018 07:09:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38317 via esterification. Among them, compounds 2e (IC₅₀ =105 nM) and 3b (IC₅₀ =114 nM) displayed excellent ACE inhibitory activity in vitro, and exhibited non-toxic to H9c2 cells. The interactions between ACE and compounds were predicted by molecular docking respectively. In verapamil-induced zebrafish HF model, the activity assay showed that these two derivatives could improve cardiovascular physiological indexes including heart beats, venous congestion, heart dilation, cardiac output, ejection fraction and fractional shortening in a dose-dependent manner. A UPLC-QTOF-MS-based serum metabolomics approach was applied to explore the latent mechanism. A total of 25 differentiated metabolites and 8 perturbed metabolic pathways were identified. These results indicated that pyxinol fatty acid ester derivatives 2e and 3b might be considered as potent drug candidates against heart failure and deserved further research and development.]]> Mon 29 Jan 2024 18:52:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51252 45° for tested four black soils, indicating that atrazine residue had the greatest P-limitation on soil microorganisms. Interestingly, microbial C- and P-limitations with different atrazine concentrations showed a strong linear relationship, especially in Qiqihar and Nongan soils. Atrazine treatment significantly negatively affected microbial metabolic limitation. Soil properties and EES interaction explained up to 88.2% for microbial C-/P-limitation. In conclusion, this study confirms the EES as a useful method in evaluating the effects of pesticides on microbial metabolic limitations.]]> Mon 28 Aug 2023 12:28:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55404 Mon 27 May 2024 12:04:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47560 Mon 23 Jan 2023 13:04:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38228 Haemophilus influenzae (NTHi) infection drives the development of steroid-resistant allergic airway disease (SRAAD), exacerbates clinical symptoms, worsens quality of life, and accounts for most of the related healthcare burden. The poor understanding of the pathogenesis of SRAAD deters the development of more effective therapeutic strategies. Here, we established a murine model of NTHi infection-induced exacerbation of allergic airway disease. We showed that NTHi infection drove Th 17-mediated pulmonary neutrophilic inflammation, aggravated airway hyper-responsiveness, and upset the balance of MUC5AC and MUC5B expression. Dexamethasone treatment effectively inhibited the features of allergic airway disease but failed to reduce NTHi-induced exacerbation, which was associated with the hyper-phosphorylation of p38 mitogen-activated protein kinase (MAPK). Interestingly, inhibition of p38 using a specific inhibitor (SB203580) only partly suppressed the airway hyper-responsiveness and mucus hyper-secretion but failed to abrogate the infection-induced neutrophilic inflammatory response in SRAAD. However, SB203580 and dexamethasone co-treatment substantially suppressed all the features of NTHi-induced SRAAD. Our findings highlight the importance of p38 MAPK in the pathogenesis of NTHi-induced steroid resistance, and this combined treatment approach may be a novel strategy against steroid-resistant asthma.]]> Mon 16 Aug 2021 16:15:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46961 Mon 12 Dec 2022 12:42:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40598 Fri 15 Jul 2022 11:21:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51551 Fri 08 Sep 2023 15:06:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40000 Fri 01 Jul 2022 14:31:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32243 Fri 01 Apr 2022 09:27:10 AEDT ]]>