INT49105
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Accordingly, perivascular T cell accumulation was most pronounced at sites of local VCAM-1 mRNA expression. | |||||||||||||||
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In the acute phase of experimental autoimmune encephalomyelitis and neuritis VCAM-1 mRNA was expressed not only on the luminal surface of inflamed vessels but also in perivascular cells suggesting a functional role of VCAM-1 in both endothelial adhesion and local restimulation of autoantigen-specific T cells. | |||||||||||||||
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Our findings of increased VCAM-1 expression during ACS and perhaps APE offer a rationale for therapeutic use of cytokine and other VCAM-1 modulators. | |||||||||||||||
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The impact of chronic transfusion therapy on VCAM-1 expression is unknown. | |||||||||||||||
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The relationship of these two variables showed strong positive correlation in which the magnitude of leukocyte infiltration into the synovial cavity was dependent on the concentration of soluble VCAM-1 produced in the blood. | |||||||||||||||
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Also, the relationship between these two variables showed a strong positive correlation (r = 0.98, p < 0.0005, df = 10) in which the magnitude of leukocyte infiltration was dependent on the concentration of soluble VCAM-1 produced in the blood.
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Tumor necrosis factor-alpha (TNF-alpha) neutralization with etanercept or infliximab treatment after induction of AIA significantly reduced both macrophage infiltration and VCAM-1 expression. | |||||||||||||||
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Vascular cell adhesion molecule-1 mRNA is expressed in immune-mediated and ischemic injury of the rat nervous system. | |||||||||||||||
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Double-stranded RNA has been shown to induce vascular cell adhesion molecule-1 (VCAM-1) protein expression on endothelial cells. | |||||||||||||||
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Recently, a new adhesion pathway has been described between VCAM-1 expressed on cytokine stimulated endothelium and the alpha 4 beta 1 integrin complex expressed on sickle reticulocytes. | |||||||||||||||
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Based on these observations, the hypothesis was developed that viral infection, through double-stranded RNA intermediates, increases endothelial VCAM-1 expression leading to sickle erythrocyte adhesion to endothelium via an alpha 4 beta 1-VCAM-1--dependent mechanism. | |||||||||||||||
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Double-stranded RNA has been shown to induce vascular cell adhesion molecule-1 (VCAM-1) protein expression on endothelial cells. | |||||||||||||||
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Additionally, VCAM-1 and ICAM-1 mRNA expressions were elevated in HYPER group suggesting endothelial activation due to vascular mechanical stretch. | |||||||||||||||
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Effect of 6-shogaol on VCAM-1 concentration in the blood of CFA treated rats | |||||||||||||||
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Determination of soluble VCAM-1 concentration in blood samples | |||||||||||||||
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These experiments demonstrate the critical role of VLA-4 in the pathogenesis of EAN and show that upregulation of VCAM-1 expression contributes, at least in part, to the progression of the disease in the early stages. | |||||||||||||||
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VCAM-1 mRNA was absent from the center of the infarcts as well as axotomized central and peripheral nerves undergoing Wallerian degeneration. | |||||||||||||||
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In addition, VCAM-1 mRNA was detected in the border zone around photochemically induced cerebral infarcts which is the predeliction site of T cell infiltration and expression of immune activation markers during the first week after ischemia. | |||||||||||||||
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Levels of sVCAM-1 were further elevated during ACS (P < 0.001) and APE (P = 0.072) and returned to the asymptomatic range on resolution. | |||||||||||||||
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Elevated plasma sVCAM-1 levels in children with sickle cell disease: impact of chronic transfusion therapy. | |||||||||||||||
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