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Kevin S. Lee

Researcher at University of Virginia

Publications -  116
Citations -  8310

Kevin S. Lee is an academic researcher from University of Virginia. The author has contributed to research in topics: Vasospasm & Ischemia. The author has an hindex of 39, co-authored 114 publications receiving 7319 citations. Previous affiliations of Kevin S. Lee include University of Virginia Health System.

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Structural and functional features of central nervous system lymphatic vessels

TL;DR: In searching for T-cell gateways into and out of the meninges, functional lymphatic vessels lining the dural sinuses are discovered, which may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.
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Unexpected role of interferon-γ in regulating neuronal connectivity and social behaviour

TL;DR: It is shown that meningeal immunity is also critical for social behaviour; mice deficient in adaptive immunity exhibit social deficits and hyper-connectivity of fronto-cortical brain regions, and suggests a co-evolutionary link between social behaviour and an anti-pathogen immune response driven by IFN-γ signalling.
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Cerebral vasospasm after subarachnoid hemorrhage: putative role of inflammation.

TL;DR: A burgeoning body of evidence suggests that various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be critical in the pathogenesis of cerebral vasospasm as mentioned in this paper.
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Inhibition of proteolysis protects hippocampal neurons from ischemia.

TL;DR: Observations indicate that calcium-activated proteolysis is an important component of the post-ischemic neurodegenerative response and that targeting this response may be a viable therapeutic strategy for preserving both the structure and function of vulnerable neurons.
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Neuroprotection with a calpain inhibitor in a model of focal cerebral ischemia.

TL;DR: The findings suggest that targeting intra- cellular, calcium-activated mechanisms, such as proteolysis, represents a viable therapeutic strategy for limiting neurological damage after ischemia.