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Diane J. Aum

Researcher at Washington University in St. Louis

Publications -  14
Citations -  337

Diane J. Aum is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Subarachnoid hemorrhage & Medicine. The author has an hindex of 6, co-authored 10 publications receiving 230 citations.

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Molecular and cellular heterogeneity: the hallmark of glioblastoma.

TL;DR: It is emphasized that each individual glioblastoma should begin to be an ensemble of molecularly distinct subclones that reflect a spectrum of dynamic cell states.
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An NAD+-dependent transcriptional program governs self-renewal and radiation resistance in glioblastoma

TL;DR: Clinical evidence that high expression of NAMPT, the rate-limiting step in NAD+ biosynthesis, in glioblastoma tumors is associated with poor overall survival in patients is provided, and a NAD+-dependent transcriptional program that governs GSC self-renewal and dictates the radiation resistance of these cells is delineated.
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Minocycline protects against delayed cerebral ischemia after subarachnoid hemorrhage via matrix metalloproteinase-9 inhibition

TL;DR: Delayed cerebral ischemia is an independent risk factor for poor outcome after aneurysmal subarachnoid hemorrhage and a role for matrix metalloproteinase‐9 in early brain injury after SAH is unclear.
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SIRT1 mediates hypoxic preconditioning induced attenuation of neurovascular dysfunction following subarachnoid hemorrhage.

TL;DR: SIRT1 mediates hypoxic preconditioning-induced protection against neurovascular dysfunction after SAH, and Resveratrol mimics this neurov vascular protection, at least in part, via SIRT1.
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Sirtuin 1 Mediates Protection Against Delayed Cerebral Ischemia in Subarachnoid Hemorrhage in Response to Hypoxic Postconditioning.

TL;DR: In this article, the authors found that hypoxic postconditioning (8% O2 for 2 hours) initiated 3 hours after subarachnoid hemorrhage (SAH) provides strong protection against cerebral vasospasm, microvessel thrombi, and neurological deficits.