INT63349
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Adhesion molecule (ICAM-1) expression on endothelial cells: 20,000 Endothelial cell (HDMEC, Lonza Inc., USA) per well in quadruplicate wells were treated with medium, vehicle, TNF? | |||||||||||||||
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Topical treatment with capsiate significantly decreased UVB-induced skin damage and inhibited the expression of COX-2, proinflammatory cytokines, and angiogenic factors, including platelet/endothelial cell adhesion molecule-1 and intercellular adhesion molecule-1. | |||||||||||||||
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Turnout cells expressed the endothelial markers CD31, | |||||||||||||||
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RESULTS: In a drug free group, digestion of a single tablet of aspirin resulted in a significantly (p<0.05) diminished expression of PECAM-1, GP IIb, fibrinogen binding with PAC-1 antibody, GP Ib, P-selectin, and CD151. | |||||||||||||||
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These differences reached statistical significance (p<0.05) for PECAM-1, GPIIb, and P-selectin expression. | |||||||||||||||
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METHODS: We used flow cytometry analysis to determine peripheral blood neutrophil expression of L-selectin, CD11a, CD11b, CD31, CD43, CD44, and intercellular adhesion molecule 2 (ICAM-3) surface adhesion molecules after treatment with aceclofenac, diclofenac, or dexamethasone. | |||||||||||||||
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In addition, we used immunohistochemistry to assess the expression of the vascular markers VEGF and CD31 as well as the bone formation marker ALP. | |||||||||||||||
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Immunohistochemistry plays an important role in identifying these rare entities, confirming the endothelial origin of the neoplasm with the expression of at least one of the vascular markers CD31, CD34, or factor VIII-related antigen. | |||||||||||||||
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Immunohistochemically, the neoplastic cells were positive for vimentin, smooth muscle actin, desmin and calponin, negative for S-100 protein, CD34, CD31 and cytokeratins (AE1/AE3, Cam 5.2). | |||||||||||||||
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Under these conditions, we observed the formation of colonies with spindle-like cells expressing Ve-cadherin and CD31 endothelial markers from both normal and dystrophic CD133+CXCR4+CD34- cell populations. | |||||||||||||||
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Using a human Stem Cell Gene Array, we found that the CD133+CXCR4+CD34- sorted cells expressed genes reflective of vascular progenitors, including CD31, FZD 2/3/4/7, CXCR4, LIFR, and Notch promoter 1 (data not shown). | |||||||||||||||
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Therefore, attention has inevitably turned to examinations of the influence of tobacco smoking on adhesion molecule expression by vascular endothelial cells. | |||||||||||||||
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However, although smokers had thus retained the ability to upregulate adhesion molecule expression, an integral part of the inflammatory response, other signs of smoking-induced immune dysregulation in the gingival microvasculature were apparent. | |||||||||||||||
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In summary, there is growing evidence that smoking influences tissue and cellular adhesion molecule expression profiles in several smoking-induced diseases: COPD; vascular diseases; and CIPD. | |||||||||||||||
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B activation in the upregulation of endothelial adhesion molecule expression. | |||||||||||||||
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In summary, there is growing evidence that smoking influences tissue and cellular adhesion molecule expression profiles in several smoking-induced diseases: COPD; vascular diseases; and CIPD. | |||||||||||||||
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However, a recent comparison of adhesion molecule expression profiles on leukocyte (L-selectin, VLA-4, and the three ? | |||||||||||||||
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However, although smokers had thus retained the ability to upregulate adhesion molecule expression, an integral part of the inflammatory response, other signs of smoking-induced immune dysregulation in the gingival microvasculature were apparent. | |||||||||||||||
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B activation in the upregulation of endothelial adhesion molecule expression. | |||||||||||||||
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Therefore, attention has inevitably turned to examinations of the influence of tobacco smoking on adhesion molecule expression by vascular endothelial cells. | |||||||||||||||
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