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Ewa M. Turner

Researcher at National Institutes of Health

Publications -  17
Citations -  1950

Ewa M. Turner is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Cytokine & Angiogenesis. The author has an hindex of 15, co-authored 17 publications receiving 1864 citations.

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Multiple cytokines and acute inflammation raise mouse leptin levels: potential role in inflammatory anorexia.

TL;DR: Leptin levels may be one mechanism by which anorexia is induced during acute inflammatory conditions, and administration of TNF, IL-1, and LIF produced a prompt and dose-dependent increase in serum leptin levels and leptin mRNA expression in fat.
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The role of interleukin 1 in growth and metastasis of human cancer xenografts.

TL;DR: The data show that the IL-1 gene is frequently expressed in metastases from patients with several types of human cancers, and may have a role alone or with other agents in the treatment ofhuman cancers.
Journal Article

Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with stage IV clear cell renal cancer.

TL;DR: Levels of endostatin are significantly elevated and correlate with VEGF levels in CCRC patients, and the nature of this correlation may lend insight into the regulation of tumor angiogenesis in patients with renal cancer.
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Interleukin-1β induced vascular permeability is dependent on induction of endothelial Tissue Factor (TF) activity

TL;DR: It is found that IL-1β induced a rapid and dose-dependent increase in TF activity in human umbilical vein endothelial cells (ECs) under routine culture conditions and modulation of TF activity may represent a strategy to treat various acute and chronic inflammatory conditions mediated by this cytokine.
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Endothelial monocyte activating polypeptide ii induces endothelial cell apoptosis and may inhibit tumor angiogenesis

TL;DR: EMAP-II appears to have important effects on angiogenesis and may play a role in regulating tumor vascular growth and induced endothelial-cell-specific apoptosis via a pathway that includes upregulation of the Fas-associated death domain and downregulation of Bcl-2.