Ion transport properties and some components of lipid structure in myocardial sarcolemma were studied under conditions of short-term acute ischemia simulated in rabbits by means of intravenous administration of vasopressin at a dose of 0.2 U/kg. The acute coronary insufficiency was accompanied by distinct alterations in the parameters specific for calcium metabolism and transport: activity of Na+, K+-ATPase and the rate of Na+Ca2+ turnover were decreased, while 45Ca-binding ability and content of Ca2+ were increased in the myocardial sarcolemma. Alterations in lipid structure, phospholipid composition of membranes and accumulation of free fatty acids appear to be responsible for the phenomenon observed. The increased rate of calcium ions transport found may occur due to alterations in the sarcolemma structure.
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CTLA4-Ig reduces muscle fiber damage in a model of Duchenne muscular dystrophy by attenuating pro-inflammatory gene expression in myeloid lineage cells.
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Duchenne muscular dystrophy (DMD) is a lethal, muscle-wasting, genetic disease that is greatly amplified by an immune response to the diseased muscles. The mdx mouse model of DMD was used to test whether the pathology can be reduced by treatments with a CTLA4-Ig fusion protein that blocks costimulatory signals required for activation of T-cells. CTLA4-Ig treatments reduced mdx sarcolemma lesions and reduced the numbers of activated T-cells, macrophages and antigen presenting cells in mdx muscle and reduced macrophage invasion into muscle fibers.
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