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Página 1 a partir de 2083 resultados
Cytoprotective effects of adenosine and inosine in an in vitro model of acute tubular necrosis.
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OBJECTIVE
We have established an in vitro model of acute tubular necrosis in rat kidney tubular cells, using combined oxygen-glucose deprivation (COGD) and screened a library of 1280 pharmacologically active compounds for cytoprotective effects.
METHODS
We used in vitro cell-based, high throughput,
Expression of thrombomodulin by smooth muscle cells in culture: different effects of tumor necrosis factor and cyclic adenosine monophosphate on thrombomodulin expression by endothelial cells and smooth muscle cells in culture.
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Thrombomodulin (TM), a critical component of the protein C anticoagulant pathway, has previously been localized to endothelial cells (EC), but not smooth muscle cells (SMC) of the blood vessel wall. We demonstrate that cultured rat, bovine, as well as human SMC, but not blood vessel wall smooth
The specific type IV phosphodiesterase inhibitor rolipram combined with adenosine reduces tumor necrosis factor-alpha-primed neutrophil oxidative activity.
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Monocytes and macrophages produce tumor necrosis factor-alpha (TNF alpha) in response to microbial products including endotoxin. TNF alpha is a potent primer of neutrophil (PMN) oxidative activity. Certain xanthine phosphodiesterase (PDE) inhibitors such as pentoxifylline have been shown to inhibit
Renal tubule necrosis and apoptosis modulation by A1 adenosine receptor expression.
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We have shown that A1 adenosine receptors (A1ARs) are cytoprotective against renal tubular necrosis and apoptosis both in vivo and in vitro. To study the role of A1AR numbers on renal epithelial cell survival, we stably overexpressed the human A1 receptor in a porcine renal tubule cell line and
The role of adenosine receptors in regulating production of tumour necrosis factor-alpha and chemokines by human lung macrophages.
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OBJECTIVE
Adenosine is a major endogenous regulator of macrophage function, and activates four specific adenosine receptors (A(1), A(2A), A(2B) and A(3)). Here, we have assessed in human lung macrophages the modulation of the expression of adenosine receptor mRNA by lipopolysaccharide (LPS), and the
Chemoattractant-induced release of elastase by tumor necrosis factor-primed human neutrophils: auto-regulation by endogenous adenosine.
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OBJECTIVE
In the present work, we studied the role of cell-derived adenosine in both the physiologic regulation and pharmacologic control of the exocytosis of azurophilic granules of neutrophils exposed to tumor necrosis factor alpha (TNF) and stimulated with some chemoattractants.
METHODS
Human
Quantitative analysis of the effect of ATP-MgCl2 and adenosine-MgCl2 on the extent of necrosis in rat liver after ischemia.
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The effect of the administration of ATP-MgCl2 and adenosine-MgCl2 on the volume density of necrosis occurring 24 hr following 60 min of ischemia in rat liver has been studied. The extent of necrosis in the lobes submitted to ischemia has been assayed by morphometric analysis of fresh liver slices
Regulation of A2B adenosine receptor functioning by tumour necrosis factor a in human astroglial cells.
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Low-affinity A2B adenosine receptors (A2B ARs), which are expressed in astrocytes, are mainly activated during brain hypoxia and ischaemia, when large amounts of adenosine are released. Cytokines, which are also produced at high levels under these conditions, may regulate receptor responsiveness. In
Adenosine-enhanced ischemic preconditioning modulates necrosis and apoptosis: effects of stunning and ischemia-reperfusion.
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BACKGROUND
Adenosine-enhanced ischemic preconditioning extends the protection of ischemic preconditioning by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery.
METHODS
The effects of adenosine-enhanced ischemic preconditioning on necrosis and
Endogenous adenosine down-modulates mid-trimester intraamniotic tumor necrosis factor-alpha production.
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OBJECTIVE
To determine whether adenosine in amniotic fluid down-regulates pro-inflammatory cytokine production.
METHODS
Mid-trimester amniotic fluid from 21 women was incubated ex vivo in the presence or absence of human adenosine deaminase, the enzyme that irreversibly degrades adenosine. After 24
Activation of adenosine A3 receptors on macrophages inhibits tumor necrosis factor-alpha.
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Murine macrophage-derived tumor necrosis factor alpha (TNF-alpha) gene expression has been shown to be dramatically induced by bacterial lipopolysaccharide, and to be dependent upon nuclear factor-kappa B (NF-kappa B) binding sites in its promoter for the lipopolysaccharide induction. Murine J774.1
Adenosine modulation of tumor necrosis factor-alpha-induced neutrophil activation.
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We hypothesized that adenosine, known to be release from inflammatory sites, could lessen the potentially damaging activity of neutrophils (PMN) primed by tumor necrosis factor-alpha (TNF alpha) at sites of infection. We investigated the effect of adenosine on PMN primed with cell-free medium from
Tumour necrosis factor-alpha and adenosine in endotoxin shockleading related cardiovascular symptoms.
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We have observed uncontrollable cardiogenic shock as a cardiovascular manifestation of systemic inflammatory response syndrome (SIRS) leading to death in a 62-year-old woman. The diagnosis of SIRS was based on the demonstration of endotoxinaemia, and highly elevated plasma levels of tumour necrosis
Adenosine increases interleukin 6 release and decreases tumour necrosis factor release from rat adrenal zona glomerulosa cells, ovarian cells, anterior pituitary cells, and peritoneal macrophages.
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Adenosine modifies interleukin 6 (IL-6) and tumour necrosis factor (TNF) release from immune tissues. Because adenosine alters endocrine function and endocrine cells secrete cytokines, its effects on IL-6 and TNF release from rat adrenals, ovaries, and anterior pituitaries were compared with its
Interleukin-1beta but not tumor necrosis factor-alpha potentiates neuronal damage by quinolinic acid: protection by an adenosine A2A receptor antagonist.
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Quinolinic acid is an agonist at glutamate receptors sensitive to N-methyl-D-aspartate (NMDA). It has been implicated in neural dysfunction associated with infections, trauma, and ischemia, although its neurotoxic potency is relatively low. This study was designed to examine the effects of a
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