INT25674
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
No causative ELA2 mutations were found, and therapeutic concentrations of sulphasalazine did not increase the expression of human neutrophil elastase. | |||||||||||||||
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causes accumulation of canine neutrophil elastase in the cytosolic compartments [12], and mutations in ELA2 may disrupt the AP3? | |||||||||||||||
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causes accumulation of canine neutrophil elastase in the cytosolic compartments [12], and mutations in ELA2 may disrupt the AP3? | |||||||||||||||
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Plasma levels of peptide B beta, a product of fibrin degradation by human neutrophil elastase, were approximately 15-fold higher (p less than 0.001) in patients with unstable angina or AMI (588 +/- 171 pmol/l, mean +/- SEM) compared with those in patients with stable angina (37 +/- 25 pmol/l) or control subjects (40 +/- 22 pmol/l), confirming intense in vivo neutrophil activation. | |||||||||||||||
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To examine whether this reduction is attributed to HNE depletion, cells were stimulated with either single or repeated 10 ? | |||||||||||||||
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1 production could be involved in HNE-induced 5-LOX and FLAP expression, chondrocytes were treated or not with a single addition of 10 ? | |||||||||||||||
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The PMN production of superoxide anion induced by various FMLP concentrations (10(-7), 10(-6) and 10(-5) M) was also decreased by diclofenac. | |||||||||||||||
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To prioritize our studies of the relation between protein modification and cellular responses, we constructed expression vectors containing individual response elements upstream of the luciferase gene, which we transfected into RKO cells prior to treatment with HNE. | |||||||||||||||
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Another effect of HNE, also important for cell | |||||||||||||||
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Another effect of HNE, also important for cell | |||||||||||||||
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This raises the question of the pharmacological actions of atomoxetine, which also increases extrasynaptic levels of NE and DA in the PFC. | |||||||||||||||
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Pretreatment with beraprost attenuated AGML and downregulated the expression of HNE and HO-1, while sensory denervation aggravated AGML and upregulated the expression of HNE and HO-1. | |||||||||||||||
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Increased HNE levels have also been found in the cerebellum of patients with spinocerebellar degeneration [235]. | |||||||||||||||
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After AGML, increased generation of HNE was observed in the injured mucosa and the surrounding submucosa, followed by nuclear translocation of Nrf2 and upregulation of HO-1 in the macrophages located in the margin of the injured mucosa and in the submucosa. | |||||||||||||||
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Neutrophils in acute hemarthrosis are activated and produce increased levels of reactive oxygen species, elastase and other lysosomal enzymes [18]. | |||||||||||||||
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Notably, no significant levels of CCL18 mRNA were detectable in blood PMN form RA patients (n = 9; Figure 2b), suggesting that CCL18 gene expression in SF PMN occurs as a result of the recruitment of PMN into the inflammatory milieu of the joint.
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The main findings were found seven days after SNT, when there was an increase in HNE-Michael adducts formation, total and p-Akt expression, and H(2)O(2) concentration. | |||||||||||||||
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General Comments
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