phospholipid/edema

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Phospholipid degradation and edema development in cold-injured rat brain.

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Development of brain edema following various pathological insults occurs after some delay. The mechanism of the delay is poorly understood. Using an in vivo model of cold-injury to study the time course of edema development, the present study indicates that the initiation of phospholipid degradation

The effects of pH on the interaction of anthrax toxin lethal and edema factors with phospholipid vesicles.

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Bacillus anthracis secretes three distinct proteins which interact in binary combinations to produce two toxins. The two effector moieties, edema factor (EF) and lethal factor (LF), interact competitively with the cell receptor-binding moiety, protective antigen (PA), to produce biologically

Transient pulmonary edema following adrenal infarction in a patient with primary anti-phospholipid syndrome.

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We report a patient with primary anti-phospholipid syndrome (APS) who developed pulmonary edema following sudden-onset pain in the left, lower back of the chest. Radiological examinations demonstrated fresh infarction of the left adrenal gland but no obvious thrombi in pulmonary arteries. The

Phospholipid degradation and cellular edema induced by free radicals in brain cortical slices.

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Cellular edema and increased lactate production were induced in rat brain cortical slices by xanthine oxidase and xanthine, in the presence of ferric dialdehyde, was increased 174%. Among the various subcellular fractions of brain cortex, xanthine oxidase-stimulated lipid peroxidation was highest in

Proteins and phospholipids in BAL from patients with hydrostatic pulmonary edema.

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The purpose of the present study is twofold: to evaluate alterations in total phospholipid content and individual phospholipid classes of the surfactant, and to detect markers of inflammatory reaction in bronchoalveolar lavage (BAL) from patients with hydrostatic pulmonary edema (HPE). Mechanically

Oral administration of a curcumin-phospholipid formulation (Meriva®) for treatment of chronic diabetic macular edema: a pilot study.

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OBJECTIVE The purpose of this open-label study was to investigate the effect of a curcumin-phospholipid lecithin formulation (Meriva®) on visual acuity and optical coherence tomography (OCT) retinal thickness in patients with chronic diabetic macular edema. METHODS Curcumin-phospholipid lecithin

Aggravated capillary non-perfusion after intravitreal bevacizumab for macular edema secondary to systemic lupus erythematosus and anti-phospholipid syndrome.

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A 22-year-old female with history of systemic lupus erythematosus (SLE) was referred for evaluation of decreased visual acuity in her right eye. Her best-corrected visual acuity (BCVA) at the time of presentation was 20/160. Widespread cotton wool spots and macular edema were seen on biomicroscopy.

Membrane lipids in the pathogenesis of brain edema: phospholipids and arachidonic acid, the earliest membrane components changed at the onset of ischemia.

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This chapter reviews studies concerning cellular membranes in the pathogenesis of cerebral edema. The main topics discussed are membrane lipids and the observation that the concentration of endogenous free fatty acids increases rapidly and reversibly in the brain after a single electroconvulsive

[Qualitative and quantitative changes in the phospholipid composition in experimental brain edema and during treatment with antiedema preparations].

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Hypothesis: membrane phospholipid degradation and polyunsaturated fatty acids play a key role in the pathogenesis of brain edema.

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Metabolism of pulmonary phospholipids in normal lung and during acute pulmonary edema.

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[Pulmonary phospholipids in edema (histochemical study)].

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Exogenous oxidants initiate hydrolysis of endothelial cell inositol phospholipids.

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Oxidants released from inflammatory cells contribute to the pathogenesis of acute inflammatory edema in many models. Chemically produced oxidants can reversibly alter the barrier properties of cultured endothelial and epithelial monolayers. This report examines the effects of nonlytic doses of H2O2

Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis.

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In mammals, oleic acid (OA) induces pulmonary edema (PE), which can initiate acute lung injury (ALI) and lead to acute respiratory distress syndrome (ARDS). Pulmonary surfactant (PS) plays a key role in a broad range of treatments for ARDS. The aim of the present investigation was to assess changes

Platelet involvement in rat paw edema induced by 2-methoxy-PAF.

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PAF-acether (PAF) or 2-methoxy-PAF (2-MX) caused a dose-dependent paw edema showing a 1:25 ratio between their inflammatory activities. 2-MX caused a thrombocytopenia, whereas PAF did not alter the number of these cells. Both phospholipids induced reductions in total leukocyte count. Rat

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