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Naomi L. Cook
Researcher at Uppsala University
Publications - 19
Citations - 509
Naomi L. Cook is an academic researcher from Uppsala University. The author has contributed to research in topics: Traumatic brain injury & Gene. The author has an hindex of 13, co-authored 18 publications receiving 421 citations. Previous affiliations of Naomi L. Cook include Science for Life Laboratory & The Heart Research Institute.
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Validation of reference genes for normalization of real-time quantitative RT-PCR data in traumatic brain injury
TL;DR: The use of the most stable reference genes presented here will allow more accurate normalization of gene expression data in TBI and highlight the importance of validating reference genes to be used for real‐time RT‐PCR analysis.
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Genetic regulation of gene expression and splicing during a 10-year period of human aging
Brunilda Balliu,Matthew G. Durrant,Olivia M. De Goede,Nathan S. Abell,Xin Li,Boxiang Liu,Michael J. Gloudemans,Naomi L. Cook,Kevin S. Smith,David A. Knowles,Mauro Pala,Francesco Cucca,David Schlessinger,Siddhartha Jaiswal,Chiara Sabatti,Lars Lind,Erik Ingelsson,Erik Ingelsson,Stephen B. Montgomery +18 more
TL;DR: It is demonstrated that, although the transcriptome and its genetic regulation is mostly stable late in life, a small subset of genes is dynamic and is characterized by a reduction in genetic regulation, most likely due to increasing environmental variance with age.
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Magnesium in acute and chronic brain injury: an update
TL;DR: A more complete picture is emerging of the role of magnesium in brain injury, its therapeutic potential as well the mechanisms associated with its decline.
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Myeloperoxidase-derived oxidants inhibit sarco/endoplasmic reticulum Ca2+-ATPase activity and perturb Ca2+ homeostasis in human coronary artery endothelial cells.
Naomi L. Cook,Helena M. Viola,Victor S. Sharov,Livia C. Hool,Christian Schöneich,Michael J. Davies,Michael J. Davies +6 more
TL;DR: MPO-mediated modulation of intracellular Ca(2+) levels may exacerbate endothelial dysfunction, a key early event in atherosclerosis, and be more marked in smokers because of their higher SCN(-) levels.
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Hydrazine compounds inhibit glycation of low-density lipoproteins and prevent the in vitro formation of model foam cells from glycolaldehyde-modified low-density lipoproteins
TL;DR: Inhibition of LDL glycation by interception of the reactive aldehydes that induce LDL modification prevents lipid loading and model foam cell formation in murine macrophage cells and Carbonyl-scavenging reagents, such as hydrazines, may therefore help inhibit LDL Glycation in vivo and prevent diabetes-induced atherosclerosis.