M
Mohammad I. Sabri
Researcher at Oregon Health & Science University
Publications - 60
Citations - 2053
Mohammad I. Sabri is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Acrylamide & Axon. The author has an hindex of 22, co-authored 60 publications receiving 2004 citations. Previous affiliations of Mohammad I. Sabri include Morehouse College & Environmental Molecular Sciences Laboratory.
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3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin.
TL;DR: The role of 3-NPA in the causation of the disease in China, its neurotoxic effects in animals and the potential role for this compound as a probe of selective neuronal vulnerability are discussed.
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Does a defect of energy metabolism in the nerve fiber underlie axonal degeneration in polyneuropathies
Peter S. Spencer,Peter S. Spencer,Mohammad I. Sabri,Mohammad I. Sabri,Herbert H. Schaumburg,Cyril L. Moore,Cyril L. Moore +6 more
TL;DR: Experimental studies with laboratory species have demonstrated that many toxic polyneuropathies are associated with distal and retrograde axonal degeneration occurring in vulnerable nerve fiber tracts in the central as well as the peripheral nervous system, termed central‐peripheral distal axonopathy.
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The Enlarging View of Hexacarbon Neurotoxicity
TL;DR: The Enlarging View of Hexacarbon Neurotoxicity as mentioned in this paper was the first attempt to enlarge the view of the neurotoxicity of hexacarbon neurotoxins, and was published in CRC Critical Reviews in Toxicology: Vol. 7, No. 4, pp. 279-356.
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Bioactivation of cyanide to cyanate in sulfur amino acid deficiency: relevance to neurological disease in humans subsisting on cassava.
J Tor-Agbidye,Valerie S. Palmer,Michael R. Lasarev,A M Craig,L L Blythe,Mohammad I. Sabri,Peter S. Spencer +6 more
TL;DR: Investigating the fate of potassium cyanide administered orally to rats maintained for up to 4 weeks on either a balanced diet (BD) or a diet lacking the SAAs, L-cystine and L-methionine found a strongly positive linear relationship between blood CN- and plasma OCN- concentrations.
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Studies on the biochemical basis of distal axonopathies--I. Inhibition of glycolysis by neurotoxic hexacarbon compounds.
TL;DR: The present data indicate that 2,5‐HD and M “BK block energy metabolism by inhibiting glycolysis at the site of GAPDH, which may account for the known failure ofGAPDH‐dependent axonal transport and the axonal degeneration which occurs in hexacarbon neuropathy.