INT43820
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The decrease of cGMP contents in cerebellum and hippocampus may be due to the decrease of sGC activities, but the decrease of cGMP contents in striatum and cerebral cortex may be mainly due to the increase of PDE activity. | |||||||||||||||
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expression of lining and sublining cells, were increased in the Th1 twist1 knockdown situation. | |||||||||||||||
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B subunit p65 to the twist1 promoter of repeatedly stimulated Th1 cells was evident 1 h after reactivation (Fig. 3, DE). | |||||||||||||||
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As expected from the phylogenetic conservation of the twist1 promoter, twist1 is also expressed by activated human Th cells. | |||||||||||||||
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Twist1 is not imprinted for enhanced expression in naive and CM CCR7+ Th cells. | |||||||||||||||
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The following primers were used to amplify the proximal twist1 promoter: (? | |||||||||||||||
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Induction of twist1 in Th cells depended on NF-? | |||||||||||||||
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Although highly variable, twist1 transcripts were increased by up to 400-fold, as compared with peripheral Th cells, in CD3+CD4+ cells isolated from the synovial fluid of inflamed joints of patients with rheumatoid arthritis or spondyloarthropathies, and in Th cells isolated from mucosal endoscopic biopsies and surgical specimens of patients suffering from CD or UC (Fig. 4 C and Table S2, available at http://www.jem.org/cgi/content/full/jem.20072468/DC1). | |||||||||||||||
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Twist1-specific shRNA reduced the level of activation-induced endogenous twist1 transcripts in Th1 cells to ? | |||||||||||||||
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Th cells isolated from chronically inflamed gut tissue of patients with ulcerative colitis (UC) or Crohn's disease (CD) and synovial fluid of patients with spondyloarthropathies or rheumatoid arthritis are imprinted to express high levels of twist1, which indicates a history of repeated restimulation and an involvement in the pathogenesis of the disease. | |||||||||||||||
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We compared the relevance qualification obtained for the ten selected topics in each one of the weighting methods.
1.4 Classification of evidence used for PDT | |||||||||||||||
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The Pa-PDT induced p-JNK caused down-regulation of the pro-apoptotic protein bcl-2 that facilitates the collapse of mitochondrial membrane and eventually initiates the intrinsic apoptotic pathway. | |||||||||||||||
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Verteporfin, a benzoporphyrin derivative monoacid ring A, is a photosensitising drug for photodynamic therapy (PDT) activated by low-intensity, nonheat-generating light of 689nm wavelength. | |||||||||||||||
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Sixty patients underwent PDT during the study period. | |||||||||||||||
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Therefore, after an unsuccessful single treatment with PDT alone, we thought that adding anti-VEGF treatment might increase the efficacy of PDT in the treatment of this particular kind of choroidal neovascularization. | |||||||||||||||
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Our present results suggest that PDT treatment could render Pa to become an apoptosis inducer for R-HepG2 cells as evidenced by the following observations: DNA fragmentation, a hallmark phenomenon of apoptosis [30], was only detected in Pa-treated samples with light illumination (Figure 2A); and the level of PS externalization (Figure 2B) were dramatically increased in the Pa-PDT treated R-HepG2 cells. | |||||||||||||||
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In addition, no significant increase in the tissue specific enzyme activities of liver (ALT, AST) and heart (LDH) in the blood samples of the Pa-PDT treated mice was observed when compared to those of the control group suggesting that damages of liver and heart were not observed after Pa-PDT treatment (Figure 1D). | |||||||||||||||
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Pa-mediated photodynamic therapy (Pa-PDT) on cancer cells | |||||||||||||||
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Our results support this notion where both procaspase-9 and the active caspase-9 were significantly increased in the Pa-PDT treated R-HepG2 cells, and finally trigger the activation of procaspase-3 that was started to be cleaved at 2 h after the Pa-PDT treatment (Figure 5A). | |||||||||||||||
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In the striatum and cerebral cortex the sGC activities and phosphorylation levels in vitro were significantly increased and were inhibited by PKA inhibitor. (3) The PDE activities showed no change in cerebellum and hippocampus, but in striatum and cerebral cortex PDE activities and phosphorylation levels in vitro were significantly increased and were inhibited by PKA inhibitor. (4) These changes described above were not observed in mice treated with naloxone 30 min prior to daily morphine injection. | |||||||||||||||
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