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Ewa M. Paleolog

Researcher at University of Oxford

Publications -  118
Citations -  7162

Ewa M. Paleolog is an academic researcher from University of Oxford. The author has contributed to research in topics: Angiogenesis & Arthritis. The author has an hindex of 46, co-authored 118 publications receiving 6760 citations. Previous affiliations of Ewa M. Paleolog include Imperial College London & Arthritis Research UK.

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Angiogenesis in rheumatoid arthritis

TL;DR: Although no clinical trials of anti-angiogenic therapy in RA have been reported to date, the blockade of angiogenesis – and especially of VEGF – appears to be a promising avenue for the future treatment of RA.
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Reduction of chemokine levels and leukocyte traffic to joints by tumor necrosis factor alpha blockade in patients with rheumatoid arthritis.

TL;DR: TNFalpha blockade reduces synovial expression of the chemokines IL-8 and MCP-1 and diminishes inflammatory cell migration into RA joints and confirms the hypothesis that in rheumatoid arthritis, tumor necrosis factor alpha plays a critical role in regulating leukocyte trafficking and chemokine levels.
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Modulation of angiogenic vascular endothelial growth factor by tumor necrosis factor alpha and interleukin-1 in rheumatoid arthritis.

TL;DR: Inhibition of TNFalpha and IL-1 activity in vivo could reduce the drive to new blood vessel formation, and hence pannus mass, adding to other therapeutic effects of anti-TNFalpha therapy in RA.
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Canonical pathway of nuclear factor kappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis.

TL;DR: The results demonstrate that the canonical pathway of NF-kappa B activation that involves p65, p50, c-Rel, and IKK-2 is activated in human atherosclerosis and results in selective up-regulation of major proinflammatory and prothrombotic mediators of the disease.
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Hypoxia--a key regulator of angiogenesis and inflammation in rheumatoid arthritis.

TL;DR: This Review highlights the molecular pathways activated by hypoxia, and how these pathways might interact with inflammatory signaling to promote and maintain synovitis in RA, with a particular focus on the response of macrophages to Hypoxia in the context of RA.