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Fatima El-Assaad

Researcher at University of Sydney

Publications -  25
Citations -  887

Fatima El-Assaad is an academic researcher from University of Sydney. The author has contributed to research in topics: Cerebral Malaria & Plasmodium berghei. The author has an hindex of 14, co-authored 22 publications receiving 747 citations. Previous affiliations of Fatima El-Assaad include University of New South Wales & St George's Hospital.

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Chemical alterations to murine brain tissue induced by formalin fixation: implications for biospectroscopic imaging and mapping studies of disease pathogenesis

TL;DR: The results provide strong evidence that amino acids, carbohydrates, lipids, phosphates, proteins and ions, such as Cl(-) and K(+), leach from tissue sections into the aqueous fixative medium during formalin fixation of the sections.
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Endocytosis and intracellular processing of platelet microparticles by brain endothelial cells.

TL;DR: Findings identify new processes by which PMP could modify endothelial cell phenotype and functions, involving mechanisms consistent with both phagocytosis and macropinocytotic.
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Microvesiculation and cell interactions at the brain–endothelial interface in cerebral malaria pathogenesis

TL;DR: Evidence is presented that intervention studies on MP production, via either gene knockout or pharmacological inhibition, can prevent the neurological syndrome and its associated mortality, suggesting potential new therapeutic avenues.
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Real-time imaging reveals the dynamics of leukocyte behaviour during experimental cerebral malaria pathogenesis

TL;DR: These studies define the real-time kinetics of leukocyte behaviour in the central nervous system during ECM, and reveal a significant role for Plasmodium-specific CD8+ T lymphocytes in regulating vascular pathology in this disease.
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Platelet-endothelial cell interactions in cerebral malaria: the end of a cordial understanding.

TL;DR: Evidence for infection-induced changes in platelets and endothelial cells occur in cerebral malaria, resulting in their concomitant activation, increased interactions between these two cell types, and a secondary pro coagulant or hypercoagulable state.