Electroretinogram in sucrose- and starch-fed rats.
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Biomedical subjects
Publications and source records attributed to H Freund.
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The prevalence of inherited thrombotic syndrome in the general population appears to be higher than that of inherited bleeding disorders. The most important candidates for screening are patients with unexplained venous thromboembolism at ages of less than 40 years: In 18 children and adolescents suffering from "idiopathic" vein thrombosis laboratory screening has been performed: PT, PTT, TT, platelet count, spontaneous platelet aggregation, von Willebrand factor, fibrinogen, plasminogen, antithrombin III, protein C, C1-inactivator, alpha-1-antitrypsin, alpha-1-antichymotrypsin, alpha-2-antiplasmin and alpha-2-macroglobulin. Compared to an age matched healthy control group in children with idiopathic vein thrombosis we could demonstrate in vitro platelet activation with significant enhanced platelet aggregation and elevated levels of von Willebrand factor in the onset of the disease. Antithrombin III, protein C, alpha-2-antiplasmin and alpha-2-macroglobulin were significantly decreased. These changes turned to be normal in the following 6 to 9 months. PT, PTT, TT, platelet count, plasminogen, alpha-1-antitrypsin, alpha-1-antichymotrypsin and c1-inactivator showed no alterations compared to the control. Platelet activation and alteration of platelet function in vivo and in vitro is established to initiate thrombosis. The von Willebrand's VIII molecule is involved in this step. The decreased inhibitors of the hemostatic system antithrombin III and protein C in the onset period of thrombotic diseases are discussed to be an increased turnover, whereas the decreased levels of alpha-2-antiplasmin and alpha-2-macroglobulin might be a counter-regulation to the thrombotic event, showing an "activated" fibrinolytic system.
Lipoprotein concentration and composition before and after Intralipid infusion were investigated in seven adult surgical patients receiving continuous total parenteral nutrition. Plasma samples were obtained prior to parenteral alimentation, after 7 days of glucose/amino acid solution without Intralipid, and again following 5 days of daily Intralipid. Cholesterol, triglyceride, protein, and phospholipid concentrations were determined on very low-, low-, and high-density lipoprotein from each specimen. After Intralipid very low-density lipoprotein concentration fell to 29% (p less than 0.015) of pre-Intralipid levels. There was no substantial increase in low-density lipoprotein phospholipid post-Intralipid to suggest the presence of lipoprotein-X. Plasma total triglyceride levels declined by 33% after Intralipid (p less than 0.01) and plasma total cholesterol levels rose by 40% (p less than 0.02). In our patients, in whom metabolic mechanisms were not saturated, it would appear that Intralipid was metabolized by activated lipoprotein lipase pathways, without the appearance of hyperlipidemia or abnormal lipoproteins.
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