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Ephrem Engidawork

Researcher at College of Health Sciences, Bahrain

Publications -  154
Citations -  3586

Ephrem Engidawork is an academic researcher from College of Health Sciences, Bahrain. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 32, co-authored 138 publications receiving 2859 citations. Previous affiliations of Ephrem Engidawork include Howard University & Karolinska University Hospital.

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Aberrant expression of peroxiredoxin subtypes in neurodegenerative disorders.

TL;DR: The present data indicate that differential regulation of antioxidant enzymes exist in DS, AD and PD, suggestive of the diversity as well as distinct functional roles of these proteins.
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In vivo antimalarial activity of the crude leaf extract and solvent fractions of Croton macrostachyus Hocsht. (Euphorbiaceae) against Plasmodium berghei in mice

TL;DR: The results collectively indicate that the plant has a promising antiplasmodial activity against Plasmodium berghei, which upholds the earlier in vitro findings as well as its folkloric use and could be considred as a potential source to develop new antimalarial agents.
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Molecular changes in fetal Down syndrome brain.

TL;DR: A review of the existing literature indicates that there are a series of biochemical alterations occurring in fetal Down syndrome brain that could serve as substrate for morphological changes and attempts to dissect these molecular changes and to explain how they may lead to mental retardation.
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Delayed neuronal death following perinatal asphyxia in rat

TL;DR: Nuclear chromatin fragmentation in asphyctic pups indicates a delayed post-asphyctic neuronal death, which suggests that delayed neuronal cell death following perinatal asphyxia is an active, apoptosis-like phenomenon.
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Alteration of caspases and apoptosis-related proteins in brains of patients with Alzheimer's disease.

TL;DR: The current findings showed that dysregulation of apoptotic proteins indeed exists in AD brain and support the notion that it may contribute to neuropathology of AD, and further hints that apoptosis in AD may occur via the death receptor pathway independent of cytochrome c.