INT72864
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Furthermore, AECA positive sera from patients, with or without coronary atherosclerosis displayed similar capacity of inducing E-selectin expression by endothelial cells. | |||||||||||||||
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AECA positive sera were further evaluated for its ability to promote in vitro E-selectin expression by HUVEC using a cell-based ELISA. | |||||||||||||||
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In addition, an increased E-selectin expression in lungs was also found. | |||||||||||||||
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Lungs of OVx allergic rats significantly increased the E-selectin expression, an effect prevented by estradiol but not by progesterone treatment. | |||||||||||||||
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Semiquantitative PCR revealed that E-selectin and IL-6 gene expressions were increased in rats following LPS injection, and an overdose of tamoxifen, an estrogen receptor antagonist, reversed the effect of 17beta-estradiol on E-selectin, but not its effect on IL-6. | |||||||||||||||
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Ischemic brain tissue expresses chemotactic proteins like MCP-1 [19] and microvascular endothelial cells significantly upregulate the expression of ICAM 1, vascular adhesion molecule-1 (VCAM) and E-selectin following acute ischemic cerebral injury as reported by Zhang et al. [35] and Blann et al. [4]. | |||||||||||||||
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Soluble E-selectin, ICAM-1 and VCAM-1 levels in systemic and coronary circulation in patients with variant angina. | |||||||||||||||
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Levels of soluble E-selectin were elevated in the diabetic patients in comparison with the non-diabetic patients at all measured time points: 74 +/- 10 ng/ml vs. 47 +/- 3 ng/ml, P < 0.03 at t = 0 h, 55 +/- 5 ng/ml vs. 38 +/- 2 ng/ml, P < 0.02 at t = 72 h. | |||||||||||||||
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In addition, we observed increased levels of E-selectin that may reflect higher endothelial cell activation, as an increased expression of adhesion molecules is known to reflect activation of the vascular endothelium [26]. | |||||||||||||||
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The inhibition of neutrophils to endothelial monolayer by piperine is due to its ability to block the tumor necrosis factor-alpha (TNF-alpha) induced expression of cell adhesion molecules i.e. | |||||||||||||||
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