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phospholipid/инфаркт
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Is platelet phospholipid-dependent thrombin generation altered by acute myocardial infarction or aspirin?
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The ability of unactivated and calcium ionophore activated platelets to support thrombin generation in defibrinated plasma was measured by a chromogenic substrate assay in the absence of clot formation. Platelet phospholipid-dependent thrombin generation (Platelet-TG) could be measured using
The intranasal administration of Carthamus tinctorius L. extract/phospholipid complex in the treatment of cerebral infarction via the TNF-α/MAPK pathway
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Carthamus tinctorius L.(Safflower), a herbal formula from Traditional Chinese Medicine (TCM), has been widely used for the treatment of cardio-cerebrovascular diseases, particularly cerebral infarction (CI) or cerebral ischemia-reperfusion injury. However, we know very little about the specific
[Role of combined administration of alpha-tocopherol and sodium nucleinate in normalizing the phospholipid composition of cardiac muscle in a model of myocardial infarction].
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It is shown that combined administrations of alpha-tocopherol and sodium nucleinate lead to normalization of qualitative and quantitative content of phospholipids in the myocardium of rabbits under conditions of an experimental myocardial infarction. The changes obtained are accompanied by a
Unsaturated fatty acid composition in serum phospholipids in patients in the acute phase of myocardial infarction.
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Acute myocardial infarction requiring mechanical bridge to transplantation in a patient with undiagnosed anti-phospholipid antibody syndrome.
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We present a young man who sustained an acute myocardial infarction with hemodynamic instability requiring placement of a left ventricular assist device and subsequent cardiac transplantation. Hematologic work-up revealed anti-phospholipid antibody syndrome. To our knowledge this is the first
[Changes in phospholipid metabolism in subcellular structures of cardiac muscle of rabbits with experimental myocardial infarction].
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Alteration in phospholipid turnover was studied in subcellular structures (nuclei, mitochondria, microsomes) of rabbit heart muscle within various postinfarctional periods (7, 14 and 21 days). The specificity of alterations in phospholipids as well as dissimilar direction of the alterations were
[Changes in the phospholipid-phospholipid ratio and lipid peroxidation in the heart muscle in experimental myocardial infarction before and after combined antioxidant therapy].
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Dynamics of quantitative relations between neutral and acid phospholipids in rabbit myocardium was studied with simultaneous registration of lipid free radical oxidation (estimated by malonic dialdehyde content) in NADP-dependent system of oxidation within various periods after simulation of
[Phospholipid composition of erythrocyte membranes under conditions of postmyocardial infarction cardiosclerosis].
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Changes in phospholipid composition of the erythrocyte membranes have been studied in experimental postmyocardial infarction cardiosclerosis. Erythrocyte membranes from animals with cardiosclerosis formed after experimantal occlusions of coronary arteries were characterized by significant decrease
Circulating levels of plasminogen and oxidized phospholipids bound to plasminogen distinguish between atherothrombotic and non-atherothrombotic myocardial infarction.
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Oxidized phospholipids (OxPL) are abundant in atherosclerotic plaques. They are also bound to circulating plasminogen after myocardial infarction (MI), and their binding to plasminogen may accentuate fibrinolysis. We sought to assess whether circulating levels of plasminogen and OxPL bound to
Anti-phospholipid antibodies and carotid-artery intima-media thickness in young survivors of myocardial infarction.
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BACKGROUND
Not all coronary events occur in young individuals with traditional risk factors. In recent years some authors have observed increased prevalence of elevated anti-phospholipid (aPL) antibodies in young patients with myocardial infarction. Also, thickening of the combined arterial
Liver infarction in a woman with systemic lupus erythematosus and secondary anti-phospholipid and HELLP syndrome.
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We report a 39-year-old primigravida, a case of systemic lupus erythematosus (SLE) and secondary anti-phospholipid syndrome (APS) with a smooth antenatal course who delivered by caesarean for non-reassuring foetal heart rate. On day 2 postoperatively, she developed a sudden severe colicky upper
Plasma thrombomodulin activity, tissue factor activity and high levels of circulating procoagulant phospholipid as prognostic factors for acute myocardial infarction.
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Several studies have indicated an association between haemostatic markers and acute myocardial infarction, but few or no studies refer to their activity. We studied plasma levels of 10 coagulation factors (fibrinogen, protein C, protein S, von Willebrand factor, D-dimers, factor VIIa, free tissue
Riboflavin attenuates myocardial injury via LSD1-mediated crosstalk between phospholipid metabolism and histone methylation in mice with experimental myocardial infarction.
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The underlying mechanisms responsible for the cardioprotective effects of riboflavin remain elusive. Current study tested the hypothesis that riboflavin protects injured myocardium via epigenetic modification of LSD1. Here we showed that myocardial injury was attenuated and cardiac function was
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
Fatty acid patterns of the serum phospholipids, cholesterolesters and triglycerides in patients with myocardial infarction (MI) during the acute phase and a follow-up of one year.
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We examined the fatty acid patterns of serum phospholipids, cholesterolesters, triglycerides and serum testosterone, estradiol, total cholesterol, triglycerides and HDL-cholesterol levels in the acute phase and after one, 6 and 12 months in a group of 27 male patients with myocardial infarction.
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