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salicylate/akuutti patologinen solukuolema
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 194 tuloksia
Local necrosis and interstitial nephritis due to topical methyl salicylate and menthol.
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Excessive percutaneous absorption of potentially toxic substances such as menthol and methyl salicylate may occur through local application of heat, such as the use of a heating pad. Menthol and methyl salicylate are found in nonprescription items and used for muscular and arthritic pains. This
Effects of Tumor Necrosis Factor Blocker on Salicylate-Induced Tinnitus in Mice.
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OBJECTIVE
Neuroinflammation is considered a novel mechanism for acute tinnitus. Here, we investigated the effects of a tumor necrosis factor (TNF) blocker on the gene expression of inflammatory-cytokine in the cochlea in a tinnitus animal model.
METHODS
Enbrel® (30 mg/kg, intraperitoneally (i.p.))
[Acute tubular necrosis with acute renal failure during the first month of treatment with 5-amino-salicylate (Pentasa(R))].
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We report a case of acute tubular necrosis in a patient with Crohn's disease treated by 5-amino-salicylate (Pentasa(R)) since one month. Normalization of renal biological parameters occurred rapidly after treatment withdrawal. This case raises the question of the optimal modalities of monitoring of
Salicylate blocks lipolytic actions of tumor necrosis factor-alpha in primary rat adipocytes.
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Increased systemic free fatty acids (FFA) impair insulin sensitivity. In obese and diabetic subjects, production of tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is elevated. TNF-alpha has a variety of effects by inducing inflammation, decreasing glucose utilization, and
Inhibition of tumor necrosis factor-induced p42/p44 mitogen-activated protein kinase activation by sodium salicylate.
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Tumor necrosis factor (TNF) activates both p42 and p44 mitogen-activated protein kinases (MAPK) in human FS-4 fibroblasts, cells for which TNF is mitogenic. We now show that TNF activates p42 MAPK in two cell lines whose growth is inhibited by TNF. A mutant TNF that binds only to the p55 TNF
Resistance to tobacco necrosis virus induced by salicylate in detached tobacco leaves.
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Sodium salicylate reduced both the size and viral antigen content of non-self-limiting necrotic lesions produced by tobacco necrosis virus (TNV) in detached tobacco leaves during the partly localized reaction to virus. The antiviral effect of salicylate occurred at concentrations close to the limits
Induction of stromelysin gene expression by tumor necrosis factor alpha is inhibited by dexamethasone, salicylate, and N-acetylcysteine in synovial fibroblasts.
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Proinflammatory cytokines, altered connective tissue metabolism, and overexpression of matrix metalloproteinases (MMPs) such as stromelysin compared to tissue inhibitors of metalloproteinases (TIMPs) result in synovial inflammation and erosion of arthritic cartilage. Tumor necrosis factor alpha
Salicylate enhances necrosis and apoptosis mediated by the mitochondrial permeability transition.
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Onset of the mitochondrial permeability transition (MPT) causes both necrotic and apoptotic cell death in cultured hepatocytes. Salicylate lowers the threshold for onset of the MPT. In this study, our aim was to determine whether nontoxic concentrations of salicylate potentiate MPT-mediated cell
Activation of p38 mitogen-activated protein kinase by sodium salicylate leads to inhibition of tumor necrosis factor-induced IkappaB alpha phosphorylation and degradation.
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Many actions of the proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-1 (IL-1) on gene expression are mediated by the transcription factor NF-kappaB. Activation of NF-kappaB by TNF and IL-1 is initiated by the phosphorylation of the inhibitory subunit, IkappaB, which targets
Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes.
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We have investigated the effects of acetylsalicylic acid and sodium salicylate on the LPS-induced synthesis of the pro-coagulant protein tissue factor (TF) and the pro-inflammatory protein tumor necrosis factor-alpha (TNF-alpha), as well as the prostaglandin PGE2 in human monocytes. Both drugs
Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stress-activated protein kinase activation.
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In a previous study, we demonstrated that sodium salicylate (NaSal) selectively inhibits tumor necrosis factor (TNF)-induced activation of the p42 and p44 mitogen-activated protein kinases (MAPKs) (known as extracellular signal-regulated kinases). Here we show that in normal human FS-4 fibroblasts
Sodium salicylate switches glucose depletion-induced necrosis to autophagy and inhibits high mobility group box protein 1 release in A549 lung adenocarcinoma cells.
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Sodium salicylate, the active metabolite of aspirin, has been shown to exert anti-inflammatory activities by inhibiting the expression of various pro-inflammatory factors, and has potent anti-cancer effects against a number of human cancers including colon, lung, breast and leukemia. Necrotic cell
Salicylate reduces cisplatin nephrotoxicity by inhibition of tumor necrosis factor-alpha.
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BACKGROUND
Salicylate was recently shown to provide protection against cisplatin nephrotoxicity in rats. We have demonstrated that enhanced tumor necrosis factor-alpha (TNF-alpha) production mediates, in part, cisplatin nephrotoxicity. The purpose of this study was to determine if the protective
Expression of tumor necrosis factor-α and interleukin-1β genes in the cochlea and inferior colliculus in salicylate-induced tinnitus.
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BACKGROUND
Changes in the gene expressions for tumor necrosis factor-α (TNF-α) and/or interleukin-1β (IL-1β) during tinnitus have not been previously reported. We evaluated tinnitus and mRNA expression levels of TNF-α, IL-1β, and N-methyl D-aspartate receptor subunit 2B (NR2B) genes in cochlea and
Lipopolysaccharide-inducible and salicylate-sensitive nuclear factor(s) on human tumor necrosis factor alpha promoter.
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Lipopolysaccharide (LPS) is one of the most potent trigger substances for monocytes and macrophages causing secretion of tumor necrosis factor alpha (TNF-alpha) and other inflammatory mediators. The nature of the nuclear factors involved in human TNF-alpha gene regulation is still unknown. Nuclear
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