https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 The peripheral vascular response to severe exercise in untethered dogs before and after complete heart block https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12673 Wed 11 Apr 2018 16:58:10 AEST ]]> Gpx5 protects the family jewels https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4655 Wed 11 Apr 2018 14:40:57 AEST ]]> Endothelial C-type natriuretic peptide maintains vascular homeostasis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19230 Wed 11 Apr 2018 14:36:46 AEST ]]> As the world grows: contraception in the 21st century https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4511 Wed 11 Apr 2018 13:20:14 AEST ]]> Uridine diphosphate-glucose/P2Y₁₄R axis is a nonchemokine pathway that selectively promotes eosinophil accumulation https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46635 JCI, Karcz et al. identified a mechanism involving the nucleotide sugar UDP-glucose (UDP-G) and the purinergic receptor P2Y14R in amplifying eosinophil accumulation in the lung. During type 2 inflammation, UDP-G activates P2Y14R on eosinophils, inducing the cells to move and migrate into the lung. Pharmacologically or genetically inhibiting P2Y14R on eosinophils attenuated eosinophil infiltration and AHR. Future experiments, including identifying additional type 2 factors regulating P2Y14R expression on lung eosinophils, are necessary to ascertain the impact of targeting P2Y14R as an alternative or adjunctive therapy to current type 2 biologics for the treatment of asthma.]]> Tue 29 Nov 2022 10:35:15 AEDT ]]> Airway mucins promote immunopathology in virus-exacerbated chronic obstructive pulmonary disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45554 Muc5ac-deficient (Muc5ac–/–) mice had attenuated RV-induced (RV-induced) airway inflammation, and exogenous MUC5AC glycoprotein administration augmented inflammatory responses and increased the release of extracellular adenosine triphosphate (ATP) in mice and human airway epithelial cell cultures. Hydrolysis of ATP suppressed MUC5AC augmentation of RV-induced inflammation in mice. Therapeutic suppression of mucin production using an EGFR antagonist ameliorated immunopathology in a mouse COPD exacerbation model. The coordinated virus induction of MUC5AC and MUC5B expression suggests that non-Th2 mechanisms trigger mucin hypersecretion during exacerbations. Our data identified a proinflammatory role for MUC5AC during viral infection and suggest that MUC5AC inhibition may ameliorate COPD exacerbations.]]> Tue 01 Nov 2022 11:18:46 AEDT ]]> PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55040 Thu 04 Apr 2024 13:51:52 AEDT ]]>