https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12630 Wed 11 Apr 2018 10:07:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23713 max reduction and increasing the K_M for the cofactor.]]> Tue 18 Oct 2016 16:59:59 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:666 Thu 25 Jul 2013 09:10:21 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33745 +_NE) were positively associated with POAF, whereas DA (p = 0.0034) levels in the 4th quartile (Q4⁺_NE) were inversely associated with POAF. Adjusting for age, heart failure (HF), and history of atrial fibrillation, the composite pre-operative (adrenergic) plasma marker (Q4⁺_NE V Q4^-_DA) was associated with a 4-fold increased occurrence of POAF (adjusted p = 0.0001). No association between plasma MAO-B and POAF was observed. Conclusions: Our results suggest that pre-operative adrenergic tone is an important factor underlying POAF. This information provides evidence that assessment of plasma catecholamines may be a low-cost method that is easy to implement for predicting which patients are likely to develop POAF. More investigation in a multicentric setting is needed to validate our results.]]> Thu 17 Feb 2022 09:31:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20802 h1 differentiator and leukocyte activator. Ample studies showed suppression of IL-12 production by numerous stress factors, including prostaglandins, catecholamines, glucocorticoids, and opioids, but did so in vitro and in the context of artificial leukocyte activation, not simulating the in vivo setting. In a recent study we reported in vivo suppression of plasma IL-12 levels by behavioral stress and surgery. The current study aims to elucidate neuroendocrine mechanisms underlying this phenomenon in naïve F344 rats. To this end, both adrenalectomy and administration of specific antagonists were used, targeting the aforementioned stress factors. The results indicated that corticosterone and prostaglandins are prominent mediators of the IL-12-suppressing effects of stress and surgery, apparently through directly suppressing leukocyte IL-12 production. Following surgery, endogenous prostaglandins exerted their effects mainly through elevating corticosterone levels. Importantly, stress-induced release of epinephrine or opioids had no impact on plasma IL-12 levels, while pharmacological administration of epinephrine reduced plasma IL-12 levels by elevating corticosterone levels. Last, a whole blood in vitro study indicated that prostaglandins and corticosterone, but not epinephrine, suppressed IL-12 production in non-stimulated leukocytes, and only corticosterone did so in the context of CpG-C-induced IL-12 production. Overall, the findings reiterate the notion that results from in vitro or pharmacological in vivo studies cannot indicate the effects of endogenously released stress hormones under stress/surgery conditions. Herein, corticosterone and prostaglandins, but not catecholamines or opioids, were key mediators of the suppressive effect of stress and surgery on in vivo plasma IL-12 levels in otherwise naïve animals.]]> Sat 24 Mar 2018 08:05:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5331 Sat 24 Mar 2018 07:45:55 AEDT ]]>