INT11359
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
As shown in Table 3, tumor size, age categories and PAI-1 mRNA expression are of prognostic value for MFS while lymph node status, histological type, histological grade and uPA expression did not add significant independent prognostic information. | |||||||||||||||
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More recently, Castello et al. [31] developed a quantitative real-time RT-PCR assay and showed that uPA and PAI-1 mRNA expression increased with tumor severity in breast cancer, thereby confirming previous results obtained by Northern blotting [32]. | |||||||||||||||
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Moreover, it has been demonstrated that high uPA and PAI-1 mRNA expression was significantly associated with shorter disease-free survival in a population of 130 primary breast cancers independent of the hormone receptor and the lymph node status [33]. | |||||||||||||||
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The independent relationship of uPA and PAI-1 gene expression with MFS was also studied using Cox-multivariate regression analysis. | |||||||||||||||
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Interestingly, uPA and PAI-1 mRNA expression may also be considered as significant prognostic factors with strong p-values (p = 0.0005 and p < 0.0001 respectively). | |||||||||||||||
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Celecoxib caused phosphorylation of eukaryotic translation initiation factor 2 kinase (PERK) and eukaryotic initiation factor-2alpha (eIF2alpha) and production of activating transcription factor (ATF)4 mRNA. | |||||||||||||||
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The expression level of uPA mRNA and the amount of uPA antigen increased significantly on treatment with each concentration of IL-1beta (1 and 10 ng/ml) and 10 ng/ml TNF-alpha. | |||||||||||||||
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In acute inflammatory condition, little is known about the expression of the urokinase-type plasminogen activator (uPA) and its receptor (uPAR) in the gastric fibroblasts. | |||||||||||||||
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The effect of indomethacin on uPA and uPAR expression in these cells was also examined. | |||||||||||||||
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To clarify the role of human gastric fibroblasts in acute inflammatory conditions such as gastric ulcer, the effects of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha on the expression of uPA and uPAR, which were suggested to be associated with tissue remodeling, in gastric fibroblasts were investigated. | |||||||||||||||
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Furthermore, we investigated the role of prostaglandin E2 (PGE2), which is suggested to play major roles in acute inflammation of the stomatch, on uPA and uPAR expression in gastric fibroblasts. | |||||||||||||||
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When gastric fibroblasts were treated with 50 microM indomethacin, the expression level of uPA mRNA decreased significantly, and the amount of uPA antigen in the culture medium and on cell surfaces decreased significantly with indomethacin in a dose-dependent manner. | |||||||||||||||
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These results suggest that uPA and uPAR expression in gastric fibroblasts is involved in the regulating system of PGE2 and that NSAIDs may delay healing of gastric mucosal injury in part through suppressing uPA production via inhibition of endogenous PG production. | |||||||||||||||
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Effects of nonsteroidal anti-inflammatory drugs on the expression of urokinase plasminogen activator and inhibitor and gelatinases in the early osteoarthritic knee of humans. | |||||||||||||||
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OBJECTIVES: The purpose of this study was to examine the ex vivo effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the expression of urokinase-type plasminogen activator (u-PA), PA inhibitor-1 (PAI-1) and gelatinases [matrix metalloproteinase (MMP)-2 and MMP-9] in the early knee osteoarthritis (OA) of humans. | |||||||||||||||
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The CSF concentrations of uPA and MMP-9 were evaluated in 30 EOMA patients and 10 controls. | |||||||||||||||
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The suppressive action of the two drugs on the synthesis of uPA, while stimulating PAI-1 production, may have a positive impact on the balance of plasminogen activator/inhibitor, which could help reduce cartilage catabolism.
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OBJECTIVES: To evaluate the effect of therapeutic and pharmacologic concentrations of two non-steroidal anti-inflammatory drugs (NSAIDs), nimesulide and naproxen, on the synthesis of urokinase (uPA), plasminogen activator inhibitor (PAI-1) and interleukin-6 (IL-6) in human synovial fibroblasts isolated from osteoarthritis (OA) patients. | |||||||||||||||
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METHODS: Urokinase, PAI-1, and IL-6 production were measured by specific ELISA. | |||||||||||||||
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Two NSAIDs, nimesulide and naproxen, can reduce the synthesis of urokinase and IL-6 while increasing PAI-1, in human OA synovial fibroblasts. | |||||||||||||||
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