[Hemolysis following heart valve prosthesis].
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Biomedical subjects
Publications and source records attributed to E Heilmann.
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The role of glycoprotein (GP) IIb-IIIa complexes and of adhesive proteins in mediating platelet aggregation is now well defined. However, less is known of the changes that occur once aggregation has begun. We report immunogold staining of thin sections of platelets or platelet aggregates, embedded in Lowicryl K4M, after the use of polyclonal antibodies to GP IIb or GP IIIa, fibrinogen (Fg), von Willebrand factor (vWF), and thrombospondin (TSP). Bound immunoglobulin G (IgG) was located by species-specific anti-IgG coupled to 5-nm gold particles and by electron microscopy. Initial experiments with platelet-rich plasma confirmed the feasibility of visualizing adhesive proteins between platelets in aggregates. Experiments then continued, using stirred suspensions of washed platelets incubated with alpha-thrombin. After 20 seconds, platelets were in contact without detectable release, although giant secretory vesicles containing adhesive proteins were seen. Internal pools of GP IIb-IIIa were progressively externalized within the aggregate. Secreted Fg was readily detected between platelets at 40 seconds. After 3 minutes, when most of the secretion had occurred, Fg had a patchwork-like distribution within the aggregate. After 6 minutes, zones with closely interspaced surface membranes, usually representing pseudopods, were dominant and Fg free. Results for vWF and TSP were similar to those for Fg. Nonetheless, GP IIb-IIIa complexes continued to be located between adjacent surface membranes throughout the aggregate. Thrombin-induced platelet aggregates were isolated, and sodium dodecyl sulfate-soluble extracts were obtained. Western blot experiments showed that, although fibrinopeptide A had been cleaved, degradation of adhesive proteins by platelet proteases had not occurred. These results emphasize that a platelet aggregate is a dynamic structure and suggest that not all surface-contact interactions are mediated by Fg or the other adhesive proteins tested in this study.
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In a retrospective study 117 patients with chronic lymphatic leukaemia (CLL) were classified according to Rai and analyzed with regard to their survival time. With increasing severity of the stage of the disease the prognosis becomes worse. A change of the stage was always in the sense of progredience of CLL. Untreated patients had the longest survival time. Among the various forms of treatment, monotherapy with corticosteroids had the worst, local irradiation therapy the best prognosis.
Ten of 117 patients with chronic lymphatic leukaemia (CLL) showed malignant tumours. In 2 cases a double carcinoma was diagnosed. The frequency of carcinoma increased with the progredience of the stage of disease classified according to Rai et al. The observations of the authors are compared with data published in the literature.