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Nabil J. Alkayed

Researcher at Oregon Health & Science University

Publications -  172
Citations -  8375

Nabil J. Alkayed is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Epoxide hydrolase 2 & Ischemia. The author has an hindex of 48, co-authored 156 publications receiving 7560 citations. Previous affiliations of Nabil J. Alkayed include Johns Hopkins University School of Medicine & University of Texas Southwestern Medical Center.

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Gender-Linked Brain Injury in Experimental Stroke

TL;DR: It is concluded that endogenous estrogen improves stroke outcome during vascular occlusion by exerting both neuroprotective and flow-preserving effects.
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Neuroprotective effects of female gonadal steroids in reproductively senescent female rats.

TL;DR: It is concluded that the protection against ischemic brain injury found in young adult female rats disappears after reproductive senescence in middle-aged females and that ovarian hormones alleviate stroke injury in reproductively senescent female rats by a blood flow-independent mechanism.
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17β-Estradiol Reduces Stroke Injury in Estrogen-Deficient Female Animals

TL;DR: Long-term estradiol replacement within a low physiological range ameliorates ischemic brain injury in previously ovariectomized female rats, and this mechanism may not be identical and depends on long-term hormone augmentation in the female.
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Functional Hyperemia in the Brain Hypothesis for Astrocyte-Derived Vasodilator Metabolites

TL;DR: Evidence is provided that the arachidonic acid released on stimulation of glutamate receptors within astrocytes is metabolized by cytochrome P450 2C11 cDNA enzymes into EETs, which act as potent dilators of cerebral vessels and are released in response to glutamate receptor activation within astracytes.
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Molecular Characterization of an Arachidonic Acid Epoxygenase in Rat Brain Astrocytes

TL;DR: A role for astrocytes in the control of cerebral microcirculation mediated by P450 2C11-catalyzed conversion of AA to EETs is suggested and the mechanism of EET-induced dilation of rat cerebral microvessels may involve activation of K+ channels.