INT224529
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
This support mechanism becomes dysregulated in aging cartilage, where extracellular PPi excess, mediated in part by upregulated NPP1 expression stimulates calcification. | |||||||||||||||
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Osteoblasts and chondrocytes have particularly high levels of both NPP1 expression and NPP specific activity [19, 46, 47]. | |||||||||||||||
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induces both NPP1 expression and elevation of extracellular PPi [12, 31, 43]. | |||||||||||||||
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induces both NPP1 expression and elevation of extracellular PPi [12, 31, 43]. | |||||||||||||||
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This model presents mechanisms underlying the common association of extracellular PPi excess with both CPPD and HA crystal deposition in OA and chondrocalcinosis cartilages, as well as the paradoxical association of extracellular PPi deficiency (from defective ANK or PC-1/NPP1 expression) with pathologic calcification of articular cartilage with HA crystals in vivo. | |||||||||||||||
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This model presents mechanisms underlying the common association of extracellular PPi excess with both CPPD and HA crystal deposition in OA and chondrocalcinosis cartilages, as well as the paradoxical association of extracellular PPi deficiency (from defective ANK or PC-1/NPP1 expression) with pathologic calcification of articular cartilage with HA crystals in vivo. | |||||||||||||||
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This model presents mechanisms underlying the common association of extracellular PPi excess with both CPPD and HA crystal deposition in OA and chondrocalcinosis cartilages, as well as the paradoxical association of extracellular PPi deficiency (from defective ANK or PC-1/NPP1 expression) with pathologic calcification of articular cartilage with HA crystals in vivo. | |||||||||||||||
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This support mechanism becomes dysregulated in aging cartilage, where extracellular PPi excess, mediated in part by upregulated NPP1 expression stimulates calcification. | |||||||||||||||
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This model presents mechanisms underlying the common association of extracellular PPi excess with both CPPD and HA crystal deposition in OA and chondrocalcinosis cartilages, as well as the paradoxical association of extracellular PPi deficiency (from defective ANK or PC-1/NPP1 expression) with pathologic calcification of articular cartilage with HA crystals in vivo. | |||||||||||||||
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mol of p-NPTMP for nucleotide pyrophosphatase phosphodiesterase (NPPase) activity or for 2.5 hours with 5 ? | |||||||||||||||
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Osteoblasts and chondrocytes have particularly high levels of both NPP1 expression and NPP specific activity [19, 46, 47]. | |||||||||||||||
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Effects of beta-escin after different periods of pre-treatment in the murine PCA model | |||||||||||||||
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To initiate the PCA reaction, 2.5 ? | |||||||||||||||
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However, at 6 h after antigen challenge, IgE-dependent PCA reactions in ears that had been engrafted with CCRL2 KO mast cells contained ? | |||||||||||||||
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However, at 6 h after antigen challenge, IgE-dependent PCA reactions in ears that had been engrafted with CCRL2 KO mast cells contained ? | |||||||||||||||
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However, at 6 h after antigen challenge, IgE-dependent PCA reactions in ears that had been engrafted with CCRL2 KO mast cells contained ? | |||||||||||||||
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General Comments
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