INT90926
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We compared the neuroprotective activity of S- and R-enantiomers of flurbiprofen and ibuprofen in a standard assay where secretions from activated human THP-1 or microglial cells are toxic to neuroblastoma SH-SY5Y cells. | |||||||||||||||
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While other genes may also increase in addition to Gli2 and PTHrP, we found minimal changes in many of the genes identified previously to be associated with metastasis to bone [29]. | |||||||||||||||
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All the other mNSAIDs, including nimesulide (NIM-03), fluosulide (CGP28238), FK3311 and NS398, also rescued THP-1 from Leu-OME mediated killing, although to a lesser degree. | |||||||||||||||
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Inhibition of L-leucine methyl ester mediated killing of THP-1, a human monocytic cell line, by a new anti-inflammatory drug, T614. | |||||||||||||||
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While it inhibits protein kinase A (PKA-) mediated phosphorylation, it also stabilizes GLI2. | |||||||||||||||
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Stimulation of the THP-1 cells with a kappa-opioid receptor-selective agonist exerted a Gi-dependent activation of c-Jun N-terminal kinase (JNK). | |||||||||||||||
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Stimulation of THP-1 with PHA was therefore used in the subsequent transfection experiments. | |||||||||||||||
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To assess the role of survivin in the inflammatory process, the human mononuclear cell line THP-1 was transfected with oligonucleotides targeting different regions of survivin mRNA. | |||||||||||||||
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THP-1 cells then were subjected to the experimental conditions described or were differentiated into adherent macrophages (phorbol dibutyrate, 0.3 ? | |||||||||||||||
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factor, can induce THP-1 apoptosis and necrosis by inducing PPAR? | |||||||||||||||
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THP-1 macrophages showed a significant increase in foam cell transformation in the presence of NS398 compared to control (78.9% ± 4.4% at 10 ? | |||||||||||||||
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In addition, CRLPs lacking apoB48, but containing apoE from the appropriate species, have been found to have effects which mimic those of physiological remnants in rat hepatocytes and pig endothelial cells [23,35], and our earlier work has shown that CRLPs cause extensive lipid accumulation in THP-1 macrophages and human monocyte derived macrophages (HMDM) which is comparable to that found in experiments with physiological CMR from rats and the murine macrophage cell line J774 [24,36]. | |||||||||||||||
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B transcriptional activation in both Raw 264.7 cells (Fig. 4A) and THP-1 cells (Fig. 4B) by 20 ? | |||||||||||||||
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General Comments
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