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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
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
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
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
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
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
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.
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
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
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
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