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Thomas J. Evans

Researcher at University of Glasgow

Publications -  166
Citations -  14472

Thomas J. Evans is an academic researcher from University of Glasgow. The author has contributed to research in topics: Nitric oxide synthase & Medicine. The author has an hindex of 48, co-authored 143 publications receiving 13144 citations. Previous affiliations of Thomas J. Evans include Marine Biological Laboratory & Royal Hospital for Sick Children.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Cyclin: A protein specified by maternal mRNA in sea urchin eggs that is destroyed at each cleavage division

TL;DR: Eggs of the sea urchin Lytechinus pictus and oocytes of the surf clam Spisula solidissima also contain proteins that only start to be made after fertilization and are destroyed at certain points in the cell division cycle, and it is proposed to call these proteins the cyclins.
Journal Article

Inducible nitric oxide synthase is present within human atherosclerotic lesions and promotes the formation and activity of peroxynitrite.

TL;DR: It is demonstrated that stimulated expression of iNOS is associated with atherosclerosis and that the activity of this enzyme under such conditions preferentially promotes the formation and activity of peroxynitrite.
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Cyclooxygenase-2 Is Widely Expressed in Atherosclerotic Lesions Affecting Native and Transplanted Human Coronary Arteries and Colocalizes With Inducible Nitric Oxide Synthase and Nitrotyrosine Particularly in Macrophages

TL;DR: Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.