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Amelia J. McFarland

Researcher at Griffith University

Publications -  22
Citations -  804

Amelia J. McFarland is an academic researcher from Griffith University. The author has contributed to research in topics: Pyocyanin & Statin. The author has an hindex of 12, co-authored 21 publications receiving 554 citations. Previous affiliations of Amelia J. McFarland include University of Texas at Dallas.

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Cellular Effects of Pyocyanin, a Secreted Virulence Factor of Pseudomonas aeruginosa.

TL;DR: It has been postulated that, given its chemical properties, PCN is able to readily cross biological membranes, however studies have yet to be undertaken to evaluate this effect, and this review highlights the possible manifestations of PCN exposure.
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Molecular mechanisms underlying the effects of statins in the central nervous system

TL;DR: An updated discussion on the molecular mechanisms contributing to statins’ possible effects on cognitive function, neurodegenerative disease, and various neurological disorders such as stroke, epilepsy, depression and CNS cancers is provided.
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Neurobiology of SARS-CoV-2 interactions with the peripheral nervous system: implications for COVID-19 and pain

TL;DR: In this paper, the authors discuss how COVID-19 may interact with the peripheral nervous system to cause pain in the early and late stages of the disease and the implications of this potential neurotropism.
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Enhanced availability of serotonin increases activation of unfatigued muscle but exacerbates central fatigue during prolonged sustained contractions

TL;DR: This is the first in vivo human study to provide evidence that 5‐HT released onto the motoneurones could play a role in central fatigue.
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Inhibition of autophagy by 3-methyladenine protects 1321N1 astrocytoma cells against pyocyanin- and 1-hydroxyphenazine-induced toxicity

TL;DR: This study provides the first evidence on mechanisms underlying the toxicity of both pyocyanin and 1-hydroxyphenazine to astrocytoma cells and provides novel evidence suggesting that this toxicity may be mediated by the formation of acidic vesicular organelles, a hallmark of autophagic cell death.