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Arduino A. Mangoni

Researcher at Flinders Medical Centre

Publications -  397
Citations -  10350

Arduino A. Mangoni is an academic researcher from Flinders Medical Centre. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 42, co-authored 348 publications receiving 7835 citations. Previous affiliations of Arduino A. Mangoni include University of Cambridge & King's College London.

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Human dimethylarginine dimethylaminohydrolase 1 inhibition by proton pump inhibitors and the cardiovascular risk marker asymmetric dimethylarginine: in vitro and in vivo significance.

TL;DR: The lack of significant associations between PPIs and ADMA in HCS participants questions the significance of DDAH1 inhibition as a mechanism explaining the increased cardiovascular risk reported with PPI use.
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Increased kynurenine plasma concentrations and kynurenine-tryptophan ratio in mild-to-moderate chronic obstructive pulmonary disease patients.

TL;DR: Kyn and Kyn/Trp ratio might represent a new, sensitive, biomarker of systemic inflammation in COPD patients and was independently associated with COPD severity.
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Blood global DNA methylation is decreased in non-severe chronic obstructive pulmonary disease (COPD) patients.

TL;DR: The presence and severity of COPD is associated with progressively lower DNA methylation in blood, however, this epigenetic alteration seems independent of oxidative stress.
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Plasma erythromycin concentrations predict feeding outcomes in critically ill patients with feed intolerance

TL;DR: In critically ill feed-intolerant patients, there is an inverse relationship between plasma erythromycin concentrations and the time to loss of clinical motor effect, which suggests that eryhromycin binding to motilin receptors contributes to variations in the duration of prokinetic response.
Journal Article

Aldosterone glucuronidation inhibition as a potential mechanism for arterial dysfunction associated with chronic celecoxib and diclofenac use in patients with rheumatoid arthritis.

TL;DR: Celecoxib has a greater potency for AGI than diclofenac and its use is associated with a significantly higher AIX%, which supports AGI as a plausible mechanism for the CV toxicity of NSAIDs.