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myristic acid/necrosis
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Pagina 1 a partire dal 32 risultati
Protective effect of myristic acid on renal necrosis occurring in rats fed a methyl-deficient diet.
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Weanling rats fed a methyl-deficient diet develop acute renal failure, the morphological features of which vary from focal tubular necrosis to widespread cortical necrosis. We and others have shown that coconut oil, rich in saturated fatty acids, has a renal protective effect in this experimental
Preparation and characterization of liposomal-lipophilic tumor necrosis factor.
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The liposomal delivery of recombinant human tumor necrosis factor (rHuTNF) has been shown to be effective in reducing its toxic effects and in its targeting of organs rich in cells of the reticuloendothelial system. However, native recombinant human TNF shows only poor affinity for liposomes,
Protein myristoylation in human mononclear phagocytes: modulation by interferon-gamma and tumor necrosis factor-alpha.
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Labelling of cells with [3H]myristic acid and analysis of labelled proteins by SDS-PAGE and fluorography, enabled the identification of a limited number of myristoylated proteins in human monocytes and monocyte-derived macrophages. In human monocytes, cultivated for one to three days, major
Myristic acid-modified thymopentin for enhanced plasma stability and immune-modulating activity.
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Natural albumin ligand (fatty acids)-conjugated peptides can rapidly bind to circulating albumin and form complexes to control the release of peptides. The purpose of this study was to prolong the half-life and immune-modulating effects of thymopentin (TP5) by using the albumin binding strategy. We
Tumor necrosis factor alpha modifies agonist-dependent responses in human neutrophils by inducing the synthesis and myristoylation of a specific protein kinase C substrate.
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Tumor necrosis factor alpha (TNF-alpha) and bacterial lipopolysaccharide (LPS) induce the synthesis and cotranslational myristoylation of an 82-kDa specific protein kinase C substrate in human neutrophils. The myristic acid is covalently bound via a hydroxylamine-resistant amide linkage to the
Macrophage tolerance response to Aggregatibacter actinomycetemcomitans lipopolysaccharide induces differential regulation of tumor necrosis factor-alpha, interleukin-1 beta and matrix metalloproteinase 9 secretion.
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OBJECTIVE
The lipopolysaccharide of Aggregatibacter actinomycetemcomitans, a potent stimulator of the immune system, induces the secretion of inflammatory mediators that modulate periodontal tissue destruction. In this study, we investigated the tolerance response of human macrophages to stimulation
Decreased CD3-mediated interferon-gamma production in relapsing-remitting multiple sclerosis.
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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that has been postulated to be T-cell mediated. We examined the proliferation and cytokine secretion of mononuclear cells after stimulation with OKT3 (anti-CD3) monoclonal antibody concanavalin A, or ionomycin
Thromboxane mediates neutrophil superoxide production in pregnancy.
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OBJECTIVE
We recently reported that activation of neutrophils obtained from pregnant women resulted in production of tumor necrosis factor-alpha by a thromboxane- and cyclooxygenase-2- dependent mechanism. Activated neutrophils also generate reactive oxygen species such as the superoxide anion,
An accessory role for the diacylglycerol moiety of variable surface glycoprotein of African trypanosomes in the stimulation of bovine monocytes.
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The membrane-associated form of the variable surface glycoprotein (mfVSG) from African trypanosomes is a potent macrophage activator capable of inducing production of tumor necrosis factor alpha (TNFalpha) in both bovine and murine models. Using a bovine model, we have re-investigated the hypothesis
Short-term menhaden oil rich diet changes renal lipid profile in acute kidney injury.
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Weanling male Wistar rats fed a choline-deficient diet develop acute kidney injury. Menhaden oil, which is a very important source of omega-3 fatty acids, has a notorious protective effect. The mechanism of this protection is unknown; one possibility could be that menhaden oil changes renal lipid
Porphyromonas gingivalis lipopolysaccharide induces shedding of syndecan-1 expressed by gingival epithelial cells.
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Syndecans are constitutively shed from growing epithelial cells as the part of normal cell surface turnover. However, increased serum levels of the soluble syndecan ectodomain have been reported to occur during bacterial infections. The aim of this study was to evaluate the potential of
Molecular cloning, expression and characterization of ovine TNF alpha.
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Tumour necrosis factor alpha (TNF alpha) is a cytokine with a wide range of effects on both lymphoid and non-lymphoid cell types. By hybridization with a human TNF alpha cDNA probe the corresponding ovine cDNA was isolated from a lipopolysaccharide (LPS) stimulated alveolar macrophage cDNA library.
Effect of IL-4 and IL-6 on the proliferation and differentiation of B-chronic lymphocytic leukemia cells.
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The proliferation and differentiation of purified malignant B cells from nine patients with chronic lymphocytic leukemia (B-CLL) were studied in vitro. We have demonstrated before that tumour necrosis factor alpha (TNF-alpha), in combination with low dose phorbol myristic acid (PMA) (0.1 ng/ml), can
Protective effect of alpha-melanocyte-stimulating hormone on pancreas islet cell against peripheral blood mononuclear cell-mediated cytotoxicity in vitro.
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The alpha-melanocyte-stimulating hormone (alpha-MSH) has been shown to interact with various cells of the immune and inflammatory systems and down-regulate either the production or the action of proinflammatory cytokines. In this study, we investigated the potential of alpha-MSH to prevent
Human retinal pigment epithelial cell interleukin-8 and monocyte chemotactic protein-1 modulation by T-lymphocyte products.
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OBJECTIVE
The purpose of the study was to examine the effect of T-lymphocyte products on human retinal pigment epithelial (HRPE) cell interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) secretion and gene expression.
METHODS
HRPE cells were stimulated for 2, 4, 8, or 24 hours with 20%
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