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arachidonic acid/demam
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Modulation of [cis-diaminedichloroplatinum(ii) hyperthermia] therapy by inhibitors of arachidonic-Acid metabolism.
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Previous studies have shown that hyperthermia is an effective modulator of cis-diamminedichloroplatinum(II) (CDDP) cytotoxicity. We have examined the potential of inhibitors of the arachidonic acid metabolism to increase the antitumor activity of CDDP and hyperthermia. Sulindac and diflunisal are
Complete NMR chemical shift assignments of odorant binding protein 22 from the yellow fever mosquito, Aedes aegypti, bound to arachidonic acid.
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Aedes aegypti mosquitoes are the vector for transmission of Dengue, Zika and chikungunya viruses. These mosquitos feed exclusively on human hosts for a blood meal. Previous studies have established that Dengue virus infection of the mosquito results in increased expression of the odorant binding
Arachidonic acid metabolites in the pathophysiology of thrombocytopenia and haemorrhage in acute African swine fever.
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Changes in the production of proaggregatory (thromboxane A2 and prostaglandin E2) and antiaggregatory (prostacyclin) prostaglandins by blood platelets, macrophages and endothelial cells during acute African swine fever caused by both a highly virulent virus and a less virulent virus were studied. No
Arachidonic acid and prostaglandin E2 in Malpighian tubules of female yellow fever mosquitoes.
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The fatty acid compositions of Malpighian tubules from adult females of the mosquito Aedes aegypti were determined for total lipids, phospholipids, triacylglycerols and three phospholipid fractions, namely phosphatidylcholine (PC), phosphatidylethanolamine (PE) and
Correction to: Complete NMR chemical shift assignments of odorant binding protein 22 from the yellow fever mosquito, Aedes aegypti, bound to arachidonic acid.
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The article listed above was initially published with incorrect copyright information. Upon publication of this Correction, the copyright of the article is changed to "The Author(s)". The original article has been corrected.
Contrasting actions of cycloheximide on fever caused by arachidonic acid and by pyrogen [proceedings].
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[Metabolism of arachidonic acid in the thrombocytes of patients with periodic disease].
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Washed platelets of patients with familial Mediterranean fever (FMF) were incubated with I-14C arachidonic acid (AA). Only 10% of AA were transformed into thromboxane A2, 12(S)-12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE) and 12(S)-12-hydroxy-5Z,8Z,10E-heptadecatrienoic acid (HHT), which
[A comparative evaluation of the efficacy of pharmacotherapeutic agents in hypoxia in the presence of hyperthermia].
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In conditions of acute hypoxia in the presence of hyperthermia drugs were shown to exhibit various degrees of protective activity. Antihypoxic action coupled with thermoprotective activity is manifested by beneficial affect on the course of the pathological process. It is quercitrol that proved to
Lipopolysaccharide injected into the cerebral ventricle evokes fever through induction of cyclooxygenase-2 in brain endothelial cells.
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Activation of the arachidonic acid cascade is an essential step for the development of fever during brain inflammation. We investigated the brain sites where this activation takes place by use of a rat model of brain inflammation. Intracerebroventricular administration of lipopolysaccharide but not
Effects on fluid balance induced by non-febrile intracerebroventricular infusions of PGE2, PGF2alpha, and arachidonic acid in the goat.
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Prostaglandins (PG) E2, F2 alpha (30 ng/kg . min-1) and arachidonic acid (150 and 300 ng/kg . min-1) were infused for 30 min into the lateral cerebral ventricle of conscious hydrated and non-hydrated goats. Like previously shown as concerns PGE1 PGE2 was found to inhibit the water diuresis and cause
Modification of convulsive behaviour and body temperature in mice by intracerebroventricular administration of prostaglandins, arachidonic acid and the soluble acetylsalicylic acid salt lysine acetylsalicylate.
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The effects of centrally injected prostaglandins (PGE1 and PGF2 alpha), arachidonic acid and lysine acetylsalicylate were examined on the seizure activity and temperature changes produced by pentylentetrazole (PTZ) and also on maximal electroshock (MES) seizures. PGE1 antagonised both PTZ and MES
Monoacylglycerol Lipase Regulates Fever Response.
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Cyclooxygenase inhibitors such as ibuprofen have been used for decades to control fever through reducing the levels of the pyrogenic lipid transmitter prostaglandin E2 (PGE2). Historically, phospholipases have been considered to be the primary generator of the arachidonic acid (AA) precursor pool
Inhibitors of cytochrome P-450 augment fever induced by interleukin-1 beta.
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Metabolites of cytochrome P-450 are produced in cells when arachidonic acid cascade is activated. Fever genesis depends largely on the cyclooxygenase branch of arachidonic acid cascade, which is caused by many stimuli, such as interleukin (IL)-1, IL-6, and interferon-alpha. To assess the
Oxyradical-mediated chromosome damage in patients with familial Mediterranean fever.
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Increased chromosome breakage is observed in patients with familial mediterranean fever (FMF). Their plasma contains clastogenic material inducing chromosome damage in cells from healthy persons. It is proposed that increased oxyradical generation by activated polymorphonuclear cells in blood and
Enhanced mobilization of intracellular Ca2+ induced by halothane in hepatocytes isolated from swine susceptible to malignant hyperthermia.
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Halothane, in a dose-dependent manner, induced the release of intracellular Ca2+ in hepatocytes prepared from swine. The magnitude of the release induced by halothane was greater for hepatocytes prepared from animals susceptible to malignant hyperthermia (MH) than for those from normal swine. Two
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