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Sanford P. Markey

Researcher at National Institutes of Health

Publications -  167
Citations -  15243

Sanford P. Markey is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Quinolinic acid & Kynurenine pathway. The author has an hindex of 52, co-authored 166 publications receiving 14907 citations. Previous affiliations of Sanford P. Markey include National Institute of Standards and Technology & Shimadzu Corp..

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A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

TL;DR: The N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkey provides a model that can be used to examine mechanisms and explore therapies of parkinsonism and the pathological and biochemical changes produced by NMPTP are similar to the well-established changes in patients with parkinsonistan.
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Chronic Parkinsonism secondary to intravenous injection of meperidine analogues.

TL;DR: Biogenic amines and metabolites in the cerebrospinal fluid and microscopic evaluation of the brain at necropsy were consistent with damage to aminergic neurons in the substantia nigra.
Posted Content

Open Mass Spectrometry Search Algorithm

TL;DR: The Open Mass Spectrometry Search Algorithm (OMSSA) as mentioned in this paper was designed to be faster than published algorithms in searching large MS/MS datasets for peptide identification.
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Open mass spectrometry search algorithm.

TL;DR: The Open Mass Spectrometry Search Algorithm (OMSSA), designed to be faster than published algorithms in searching large MS/MS datasets, matches more spectra from a standard protein cocktail than a comparable algorithm.
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Intraneuronal generation of a pyridinium metabolite may cause drug-induced parkinsonism.

TL;DR: It is reported here that MPTP is oxidized in the brain to a pyridinium species (a compound with potent herbicidal activity) and, in the monkey, is trapped intraneuronally and demonstrated that this enzymatic oxidation is blocked in vivo in the mouse by a monoamine oxidase inhibitor, indicating that the oxidative metabolism is required for its neurotoxic effect.