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turpentine/upala
Veza se sprema u međuspremnik
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Inflammatory competence of fetal rat: acute-phase plasma protein response of the fetus treated by turpentine in utero.
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Using crossed immunoelectrophoresis, immunoelectrodiffusion, autoradiography, and equilibrium binding techniques, we demonstrate that the rat fetus, directly challenged in utero at 18 days by a single subcutaneous turpentine injection, presents a complex acute-phase plasma inflammatory response. A
Protein metabolism in slow- and fast-twitch skeletal muscle during turpentine-induced inflammation.
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The aim of our study was to evaluate the differences in protein and amino acid metabolism after subcutaneous turpentine administration in the soleus muscle (SOL), predominantly composed of red fibres, and the extensor digitorum longus muscle (EDL) composed of white fibres. Young rats (40-60 g) were
Increase in antilipoperoxidant activity of plasma as a consequence of an inflammatory reaction induced by subcutaneous turpentine in the rabbit.
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In the rabbit, an acute inflammatory reaction triggered by the subcutaneous administration of turpentine induces in hepatic tissues an oxidative stress, as well as a decrease in activity of enzymatic scavengers of reactive oxygen species (ROS). The objective of this study was to investigate, the
Elevation of circulating monitor peptide/pancreatic secretory trypsin inhibitor-I (PSTI-61) after turpentine-induced inflammation in rats: hepatocytes produce it as an acute phase reactant.
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Monitor peptide (MP) is a trypsin-sensitive cholecystokinin (CCK)-releasing peptide purified from rat pancreatic juice on the basis of its stimulatory activity toward pancreatic enzyme secretion and has been reported to exhibit cell growth-stimulating activity. Pancreatic secretory trypsin inhibitor
Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6.
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Heme oxygenase-1 (HO-1) is the inducible isoform of an enzyme family responsible for heme degradation and was suggested to be involved in the acute phase response in the liver. However, the mechanisms of the HO-1 regulation under inflammatory conditions are poorly understood. Therefore, the purpose
The mechanism of the anti-inflammatory effect of turpentine in the rat.
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The influence of counter irritation by turpentine on carrageenan-oedema, leucocyte count, plasma kininogen stores and composition of sponge-induced exudates has been investigated in the rat. Counter irritation reduced the carrageenan-oedema in normal as well as in adrenalectomized rats. It induced
Modified immunoglobulin G glycosylation pattern during turpentine-induced acute inflammation in rats.
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Alterations in the pattern of protein glycosylation have been described during inflammation. In chronic parasitic and tumoral diseases we have reported an increase in the proportion of serum Immunoglobulin G (IgG) molecules possessing an altered Fab glycosylation pattern designated asymmetric
The effect of turpentine-induced inflammation on rat liver glycosyltransferases and Golgi complex ultrastructure.
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Turpentine-induced inflammation in the rat caused a 1.6--2.3-fold increase in liver homogenate sialyl-, galactosyl- and N-acetylglucosaminyltransferase total and specific enzyme activities. Peak transferase activities were achieved at about 40 h after turpentine injection; the rise and fall of these
Intestinal iron absorption during turpentine sterile inflammation in the rat. Influences of isoproterenol and propranolol.
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59Fe was incorporated in vivo into intestinal sacs prepared in control rats as well as in animals with turpentine sterile abscesses and 59Fe counts were detected in the intestinal wall, in blood, in liver, in spleen and in femur of animals, at different time intervals (20, 40 and 120 min) following
Increased serum antibacterial activity after turpentine-induced acute inflammation.
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An acute inflammatory response was induced in rabbits by an intramuscular injection of turpentine. After this injection serial serum samples were obtained and serum haptoglobin levels were monitored. In addition, increased antibacterial activity was measured using a viable plate and photometric
In-vitro biotransformation of antipyrine, lignocaine and propranolol in the liver of rats with turpentine-induced inflammation.
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In rats with inflammation induced by turpentine injection, changes in drug disposition occur in-vivo and in the perfused isolated liver. Therefore the biotransformation of a low extraction drug, antipyrine, and of two high extraction drugs, lignocaine and propranolol, has been evaluated in the 9000g
Effects of turpentine-induced inflammation on the hypoxic stimulation of intestinal Fe3+ absorption in mice.
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Chronic subcutaneous turpentine administration (weekly for 6 weeks) induced a mild normocytic anaemia in mice. In-vitro and in-vivo intestinal Fe3+ absorption parameters were, however, not significantly altered from values in saline-treated or untreated mice. Normal mice, when exposed to 3 days
Differential expression of cytokine genes in monocytes, peritoneal macrophages and liver following endotoxin- or turpentine-induced inflammation in rat.
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Pro-inflammatory cytokines are produced after systemic or local inflammation by a wide variety of cell types including monocytes, macrophages, Kupffer and endothelial cells. Previous studies have shown that IL-6 gene expression does not occur in liver from rats undergoing an acute phase response
Polyacrylamide gel electrophoretic patterns of chicken serum in acute inflammation induced by intramuscular injection of turpentine.
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To develop a method to detect hidden inflammation using serum protein in chickens, changes in serum proteins with acute inflammation were analyzed using a turpentine-induced inflammation model. Inflammation in the pectoral muscle of a 14-wk-old White Leghorn became apparent 3 h after the injection
Turpentine-induced inflammation reduces the hepatic expression of the multiple drug resistance gene, the plasma cholesterol concentration and the development of atherosclerosis in apolipoprotein E deficient mice.
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We aimed to investigate the effect of turpentine-induced inflammation in an atherosclerosis-prone murine model. We have induced a chronic aseptic inflammation in apolipoprotein E-deficient mice, with or without a dietary supplement of aspirin (n = 10, each), by the injection of a mixture (1:1) of
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