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Costantino Iadecola

Researcher at Cornell University

Publications -  468
Citations -  59815

Costantino Iadecola is an academic researcher from Cornell University. The author has contributed to research in topics: Stroke & Ischemia. The author has an hindex of 107, co-authored 435 publications receiving 51044 citations. Previous affiliations of Costantino Iadecola include University of Chicago & University of Minnesota.

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Fastigial stimulation increases ischemic blood flow and reduces brain damage after focal ischemia

TL;DR: FN stimulation, unlike hypercapnia, increases CBF to the ischemic cortex, improves recovery of electrical activity, and reduces tissue damage after MCA occlusion, and these findings support the hypothesis that FN stimulation reduces isChemic damage by enhancing collateral flow to theIschemic territory.
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Female protection from slow‐pressor effects of angiotensin II involves prevention of ROS production independent of NMDA receptor trafficking in hypothalamic neurons expressing angiotensin 1A receptors

TL;DR: The data suggest that the sexual dimorphism in AngII‐induced hypertension is associated with sex differences in ROS production in AT1aR‐containing PVN cells but not with postsynaptic NMDA receptor trafficking.
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Subcellular localization of nicotinamide adenine dinucleotide phosphate oxidase subunits in neurons and astroglia of the rat medial nucleus tractus solitarius: relationship with tyrosine hydroxylase immunoreactive neurons.

TL;DR: Results indicate that NADPH oxidase assembly and consequent superoxide formation are likely to occur near the plasmalemma, as well as on vesicular organelles associated with intracellular calcium storage within mNTS neurons and glia, and NADPH oxidation-derived superoxide in neurons andglia may directly or indirectly modulate catecholaminergic neuron activity in the mN TS.
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Prohibitin Viral Gene Transfer Protects Hippocampal CA1 Neurons From Ischemia and Ameliorates Postischemic Hippocampal Dysfunction

TL;DR: It is demonstrated that prohibitin overexpression protects highly vulnerable CA1 neurons from ischemic injury in vivo and suggested that the effect is mediated by reduction of postischemic reactive oxygen species generation and preservation of mitochondrial outer membrane integrity that prevents activation of apoptosis.
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Rates of Spinal Cord Infarction After Repair of Aortic Aneurysm or Dissection.

TL;DR: Adult patients discharged from nonfederal acute care hospitals in California, New York, and Florida who underwent surgical or endovascular repair of an aortic aneurysm or dissection between 2005 and 2013 are identified to estimate crude rates of spinal cord infarction (SCI).