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uridine/inflammation
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Effects of uridine, isomatitol and 4-thiouridine on in vitro cell adhesion and in vivo effects of 4-thiouridine in a lung inflammation model.
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Since leukocyte adhesion to endothelial cells is crucial for extravasation of leukocytes to sites of inflammation, inhibition of cell-cell adhesion has been suggested as a means to achieve selective modulation of the immune system. We have, using a static in vitro adhesion assay involving adhesion
Enhancement by Uridine Diphosphate of Macrophage Inflammatory Protein-1 Alpha Production in Microglia Derived from Sandhoff Disease Model Mice.
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Sandhoff disease (SD) is a lysosomal β-hexosaminidase (Hex) deficiency involving excessive accumulation of undegraded substrates, including GM2 ganglioside, and progressive neurodegeneration. Macrophage inflammatory protein-1α (MIP-1α) is a crucial factor for microglia-mediated neuroinflammation in
Mitochondrial function, inflammation, fat and bone in HIV lipoatrophy: randomized study of uridine supplementation or switch to tenofovir.
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BACKGROUND
Lipoatrophy modestly improves when the thymidine analogue nucleoside reverse transcriptase inhibitor (tNRTI) is removed. In vitro, uridine (NucleomaxX(®); Pharma Nord, Vojens, Denmark) reversed tNRTI mitochondrial toxicity.
METHODS
All patients had lipoatrophy on a tNRTI-containing
Anti-inflammatory effects of exogenous uridine in an animal model of lung inflammation.
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Nucleosides like adenosine, uridine and their nucleotide derivatives (e.g. ATP and UTP) play important roles in many cellular functions, sometimes by acting as signalling molecules through binding to specific P2 nucleotide receptors. P2 receptors are subdivided into P2X and P2Y subfamilies, the
Local administration of uridine suppresses the cardinal features of asthmatic airway inflammation.
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BACKGROUND
The immuno-modulatory properties of nucleotides such as adenosine or inosine, have been described extensively. Recently, the nucleoside uridine and its analogue 4-thiouridine have gained attention for their protective role in acute lung inflammation.
OBJECTIVE
In this study, we
The endothelium-derived contracting factor uridine adenosine tetraphosphate induces P2Y(2)-mediated pro-inflammatory signaling by monocyte chemoattractant protein-1 formation.
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It is very well established that purinergic signaling plays a relevant role in vascular physiology and pathophysiology. Recently, a new purinoceptor agonist uridine adenosine tetraphosphate (Up(4)A) has been identified as a highly potent endothelial-derived contracting factor (EDCF). The purpose of
The role of mitochondrial KATP channel in anti-inflammatory effects of uridine in endotoxemic mice.
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In this study, we examined the effects of uridine on plasma cytokine levels, heat shock protein (HSP) 72 expression, and nuclear factor (NF)-κB signaling in spleen lymphocytes after exposure of male BALB/c mice to Escherichia coli lipopolysaccharide (LPS). Mice were treated with uridine (30 mg/kg
Uridine supplementation exerts anti-inflammatory and anti-fibrotic effects in an animal model of pulmonary fibrosis.
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BACKGROUND
Pulmonary fibrosis is a progressive disease with only few treatment options available at the moment. Recently, the nucleoside uridine has been shown to exert anti-inflammatory effects in different animal models, e.g. in acute lung injury or bronchial asthma.
METHODS
Therefore, we
Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition.
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Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs
Characterization of autoantibodies against uridine-diphosphate glucuronosyltransferase in patients with inflammatory liver diseases.
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Uridine diphosphate glucuronosyltransferase (UGT) was identified as an antigenic target in a subgroup of liver-kidney microsomal autoantibodies and was termed LKM-3. To evaluate the nature of LKM-3 antibodies, we screened sera from 80 untreated patients with autoimmune hepatitis (AIH) type 1 and 2,
HISTOCHEMICAL STUDIES OF LEUKOCYTES FROM AN INFLAMMATORY EXUDATE. IV. URIDINE DIPHOSPHATE GLUCOSE-GLYCOGEN TRANSGLYCOSYLASE.
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Studies on the mechanism of action of salicylates. VII. Effect of a few anti-inflammatory agents on uridine-5'-diphosphoglucose dehydrogenase.
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[INTERVENTION OF ANTI-INFLAMMATORY AGENTS IN THE TRANSGLUCOSIDATION PHENOMENA LINKED TO URIDINE DIPHOSPHATE GLUCOSE].
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In vitro activated CD4+ T cells from interferon-gamma (IFN-gamma)-deficient mice induce intestinal inflammation in immunodeficient hosts.
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To investigate the role of IFN-gamma in the immunopathogenesis of inflammatory bowel disease (IBD), severe combined immunodeficient (SCID) mice were transplanted with in vitro activated CD4+ T cells from either wild-type (WT) or IFN-gamma-deficient (IFN-gammaKO) BALB/c mice. In vitro, the two types
Immunohistochemical study of corneal inflammation after femtosecond laser clear corneal incisions or manual surgery.
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To use immunohistochemical staining to evaluate corneal inflammation and apoptosis induced after femtosecond laser incisions or manual incisions.
Ophthalmology Clinic, University G. d'Annunzio, Chieti, Italy.
Experimental study.
Ninety human cadaver corneas were cut manually or with the femtosecond
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