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Página 1 a partir de 111 resultados
Role of phosphate, pyrophosphate, adenine nucleotides and sulfate in activating production of the superoxide radical by macrophages, and in formation of rat paw edema.
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The presence of anions of phosphate (Pi), pyrophosphate (PPi), adenine nucleotides and sulfate greatly enhanced the production of superoxide radical (-O-2) by isolated guinea-pig macrophages. These anions, however, failed to enhance the production of -O-2 by the xanthine oxidase system, suggesting
Alteration of rat lung adenine nucleotide content after pulmonary edema.
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[Correlation with lipid peroxidation, brain energy metabolism and brain edema in cerebral ischemia].
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In order to unravel possible involvement of free radical reactions and lipid peroxidation in the ischemic cell damage, chemiluminescence, energy metabolism, water content and concentrations of Na+, K+ were measured with time, using highly ischemic whole brain models of rats. The amount of
Metabolic changes in nicotinamide adenine dinucleotide in response to anthrax toxin.
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Bacillus anthracis produces a toxin both in vitro and in vivo which, when injected intravenously into rats, brings about the death of the animals accompanied by gross pulmonary edema. Lung tissue removed prior to death showed, in vitro, a 30% reduction in overall oxidative metabolism (Q(o2)),
Regulation by sulfanylurea receptor type 1 of a non-selective cation channel involved in cytotoxic edema of reactive astrocytes.
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Hypoxia-ischemia and ATP depletion are associated with cytotoxic edema of glial cells, but mechanisms involved remain incompletely characterized. We examined morphologic and electrophysiological responses of freshly isolated native reactive astrocytes (NRAs) following exposure to NaN3, which
The effects of nicotinamide adenine dinucleotide on intracerebral hemorrhage-induced brain injury in mice.
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In the present study, we investigated whether the administration of nicotinamide adenine dinucleotide (NAD+) provides brain protection in a mouse model of intracerebral hemorrhage (ICH). Male CD-1 mice were divided into sham, ICH treated with vehicle and ICH treated with NAD+ (10 or 20 mg/kg,
Regional changes in the cellular level of adenine nucleotides in ischemic rat brain subjected to single embolization.
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Regional changes in adenine nucleotides in the rat brain were studied after 1 h of ischemia produced by the embolization method. The animals were divided into three groups according to neurological symptoms: sham-operation group, group A (hemiparesis only), and group B (hemiparesis with
[Early adenine arabinoside therapy in herpes simplex encephalitis (HSE)].
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Five patients with HSE were treated with adenine arabinoside and one additional patient with cytosine arabinoside. The diagnosis of HSE was confirmed in retrospect by the rising CF titers and the Enzyme-Linked Immunosorbent Assay (ELISA) levels in CSF (Table 2). Brain biopsy was not performed. The
Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle.
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Skeletal muscle ischemia results in energy depletion and intracellular acidosis. Reperfusion is associated with impaired adenine nucleotide resynthesis, edema formation, and myocyte necrosis. The purpose of these studies was to define the time course of cellular injury and adenine nucleotide
β-Nicotinamide adenine dinucleotide attenuates lipopolysaccharide-induced inflammatory effects in a murine model of acute lung injury.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) occur in approximately 200,000 patients per year. Studies indicate that lung endothelium plays a significant role in ALI. The authors' recent in vitro studies demonstrate a novel mechanism of β-nicotinamide adenine dinucleotide
Effect of 2-chloro-substitution of adenine moiety in mixed-ligand gold(I) triphenylphosphine complexes on anti-inflammatory activity: the discrepancy between the in vivo and in vitro models.
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A series of gold(I) triphenylphosphine (PPh3) complexes (1-9) involving 2-chloro-N6-(substituted-benzyl)adenine derivatives as N-donor ligands was synthesized and thoroughly characterized by relevant methods, including electrospray-ionization (ESI) mass spectrometry and multinuclear NMR
A mutation unique in serine protease inhibitors (serpins) identified in a family with type II hereditary angioneurotic edema.
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BACKGROUND
Hereditary angioneurotic edema (HANE) is an autosomal dominant disease due to genetic alterations at the C1 inhibitor gene. Mutations within the C1 inhibitor gene are responsible for the molecular defect in type II HANE. Most of the dysfunctional proteins result from mutations involving
Structure of anthrax edema factor-calmodulin-adenosine 5'-(alpha,beta-methylene)-triphosphate complex reveals an alternative mode of ATP binding to the catalytic site.
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Anthrax edema factor (EF) is a key virulence factor secreted by Bacillus anthracis. Here, we report a structure, at 3.0 A resolution, of the catalytic domain of EF (EF3) in complex with calmodulin (CaM) and adenosine 5'-(alpha,beta-methylene)-triphosphate (AMPCPP). Although the binding of the
Protection against LPS-induced pulmonary edema through the attenuation of protein tyrosine phosphatase-1B oxidation.
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One hallmark of acute lung injury is the disruption of the pulmonary endothelial barrier. Such disruption correlates with increased endothelial permeability, partly through the disruption of cell-cell contacts. Protein tyrosine phosphatases (PTPs) are known to affect the stability of both
Different Roles of N-Terminal and C-Terminal Domains in Calmodulin for Activation of Bacillus anthracis Edema Factor.
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Bacillus anthracis adenylyl cyclase toxin edema factor (EF) is one component of the anthrax toxin and is essential for establishing anthrax disease. EF activation by the eukaryotic Ca2+-sensor calmodulin (CaM) leads to massive cAMP production resulting in edema. cAMP also inhibits the nicotinamide
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