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George A. Smythe

Researcher at University of New South Wales

Publications -  179
Citations -  8855

George A. Smythe is an academic researcher from University of New South Wales. The author has contributed to research in topics: Kynurenine pathway & Quinolinic acid. The author has an hindex of 52, co-authored 179 publications receiving 8338 citations. Previous affiliations of George A. Smythe include Garvan Institute of Medical Research & Victor Chang Cardiac Research Institute.

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Kynurenine pathway metabolism in human astrocytes: a paradox for neuronal protection

TL;DR: It is shown that kynurenine in concentrations comparable with those produced by astrocytes led to significant production of QUIN by macrophages, suggesting that astroCytes alone are neuroprotective by minimizing QUIN production and maximizing synthesis of kynurenic acid.
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Expression of indoleamine 2,3-dioxygenase and production of quinolinic acid by human microglia, astrocytes, and neurons.

TL;DR: It is found that astrocytes, neurons, and microglia expressed IDO but onlymicroglia were able to produce detectable amounts of QUIN, and the first evidence of IDO expression and lack of production ofQUIN in culture of primary human neurons is provided.
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Characterization of the kynurenine pathway in human neurons.

TL;DR: The kynurenine pathway is characterized in human neurons and the human SK-N-SH neuroblastoma cell line and it is found that the kyn Laurenine pathway enzymes were variably expressed.
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Increased nitric oxide production in heart failure

TL;DR: High-capacity inducible isoform of nitric oxide synthase is present in the myocardium of patients with idiopathic dilated cardiomyopathy and plasma nitrate was significantly increased in patients with heart failure, which may compensate for the vasoconstrictor effect of neurohumoral adaptions to heart failure.
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Fate of steroid estrogens in Australian inland and coastal wastewater treatment plants.

TL;DR: The detection of EE2 in the waste activated sludge, undetectable in the raw sewage, suggests that EE2 is resistant to biological treatment in the sequential batch reactor and is primarily removed due to sorption.