Selective inhibition of platelet thromboxane generation with low-dose aspirin does not protect rats with reduced renal mass from the development of progressive disease

Article Abstract:

Rats whose kidneys have lost mass develop high blood pressure, pass excess protein in their urine, and develop progressive glomerulosclerosis (hardening and blockage of the nerves and blood vessels which filter blood in the kidney). These changes are associated with increased output of thromboxane (plays a role in blood clotting) in the urine. Treatment with a substance that prevents thromboxane production, thromboxane synthetase inhibitor or TSI, prevents glomerulosclerosis and progressive deterioration of kidney function. It has been speculated that this occurs because TSI prevents the generation of substances that influence function of the glomerulus. Because TSI also reduces the thromboxane output of glomerular cells and lowers blood pressure, it is not known whether thromboxane itself is responsible for the glomerulosclerosis. Aspirin, which suppresses thromboxane output, had no effect on the excess of protein, nor did it reduce kidney deterioration. Mere prevention of blood clotting and thromboxane generation does not prevent glomerulosclerosis in rats with loss of kidney mass. It was concluded that the beneficial effects of TSI are due either to an effect on glomerular cell thromboxane output or to lowering blood pressure.

Prostaglandins, Kidneys, Thromboxanes, Kidney, Kidney glomerulus, Glomeruli

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Supranormal von Willebrand factor multimers in scleroderma

Article Abstract:

Scleroderma is apparently caused by pathologic production of antibodies directed against the patient's own cells and it is thus classified as an autoimmune disease. A symptom of the disease is sclerosis, the thickening of connective tissue elements of the skin and internal organs. Although not well understood, the mechanism of sclerosis involves the the ability of platelets (blood fragments which are involved in the clotting process) to cluster and adhere to one another. The von Willebrand factor, a normally occurring compound in blood which causes platelets to adhere, was measured in eleven patients with scleroderma and was found in large amounts and in unusual forms in all patients on two different occasions, nine to twelve months apart. Low doses of aspirin (40mg) caused a slight improvement in the degree of platelet adhesion, suggesting that the increased level of von Willebrand factor might be produced by the platelets. The results also suggest that the level and type of von Willebrand factor may be a causal factor in systemic scleroderma.

Causes of, Complications and side effects, Autoimmune diseases, Scleroderma (Disease), Von Willebrand's disease

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Functional consequences of an arginine180 to glutamine mutation in factor IX Hilo

Article Abstract:

The Factor IX Hilo molecule related to the other factor IX clotting factors but it has no measured effect on blood clotting. The protein is produced by a small genetic abnormality in the factor IX gene which is responsible for the production of these clotting factors. When a patient's blood contains factor IX Hilo, various aspects of the blood's ability to coagulate are affected. For example, blood shows a delayed coagulation time to prothrombin extracted from the brain of an ox. When the same blood had factor IX Hilo removed, the coagulation time returned to normal. When factor IX Hilo was added back into the blood, the clotting difficulty reappeared. The data suggest that the factor IX gene defect that gives rise to factor IX Hilo protein is responsible for disruption of normal clotting, as evidenced by the lengthened clotting time with ox brain prothrombin.

Product defects and recalls, Measurement, Hemophilia, Prothrombin, Blood coagulation factors, Mutation (Biology), Mutation, Blood clotting, Blood coagulation

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