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Ian A. Clark

Researcher at Australian National University

Publications -  184
Citations -  11276

Ian A. Clark is an academic researcher from Australian National University. The author has contributed to research in topics: Malaria & Plasmodium vinckei. The author has an hindex of 56, co-authored 183 publications receiving 10674 citations. Previous affiliations of Ian A. Clark include Animal Research Institute & The Heart Research Institute.

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Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease.

TL;DR: It is essential to expand the view of pathogenesis beyond Aβ and tau pathology and suggest several future directions for AD research, which it is argued will be critical to understanding AD pathogenesis.
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Evidence for reactive oxygen intermediates causing hemolysis and parasite death in malaria.

TL;DR: The evidence that malaria parasites are susceptible to free oxygen radicals supports the view that high intraerythrocytic oxidative stress may contribute to the high frequencies in malarial areas of genes for certain erythroCyte-related traits and suggests that some antimalarial drugs may suppress parasites partly through oxidative damage.
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Killing of Plasmodium falciparum in vitro by nitric oxide derivatives

TL;DR: In vitro susceptibility of the human malaria parasite Plasmodium falciparum to killing by nitric oxide and related molecules is investigated and nitrosothiol derivatives of cysteine and glutathione were found to be about a thousand times more active than nitrite.
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Aluminium salts accelerate peroxidation of membrane lipids stimulated by iron salts.

TL;DR: It is suggested that Al( III) ions produce an alteration in membrane structure that facilitates lipid peroxidation, and that the increased formation of fluorescent age pigments in the nervous system of patients exposed to toxic amounts of Al(III) may be related to this phenomenon.
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Human malarial disease: a consequence of inflammatory cytokine release

TL;DR: The evidence is considered that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen.