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Brian T. Hawkins

Researcher at Duke University

Publications -  54
Citations -  4816

Brian T. Hawkins is an academic researcher from Duke University. The author has contributed to research in topics: Blood–brain barrier & Tight junction. The author has an hindex of 22, co-authored 49 publications receiving 4242 citations. Previous affiliations of Brian T. Hawkins include University of Arizona & National Institutes of Health.

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Journal ArticleDOI

The Blood-Brain Barrier/Neurovascular Unit in Health and Disease

TL;DR: Understanding how BBB TJ might be affected by various factors holds significant promise for the prevention and treatment of neurological diseases.
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Increased blood–brain barrier permeability and altered tight junctions in experimental diabetes in the rat: Contribution of hyperglycaemia and matrix metalloproteinases

TL;DR: These data indicate that diabetes increases BBB permeability via a loss of tight junction proteins, and that increased BB B permeability in diabetes does not result from hyperglycaemia alone.
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Nicotine increases in vivo blood-brain barrier permeability and alters cerebral microvascular tight junction protein distribution

TL;DR: It was found that continuous administration of nicotine for 1 and 7 days led to increased permeability of the blood-brain barrier to [14C]-sucrose without significant changes in its initial volume of distribution.
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Nicotine and cotinine modulate cerebral microvascular permeability and protein expression of ZO-1 through nicotinic acetylcholine receptors expressed on brain endothelial cells.

TL;DR: Evidence is provided that nicotine and cotinine alter BBB permeability and tight junctional protein expression of ZO-1, thereby altering the BBB response to stroke conditions.
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Chronic inflammatory pain leads to increased blood-brain barrier permeability and tight junction protein alterations

TL;DR: During chronic inflammatory pain, alterations in BBB function are associated with changes in specific transmembrane TJ proteins, demonstrating that the blood-brain barrier can be modulated by disease pathologies including inflammatory pain.