Browsing by Author "Wyatt, JH"

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    A microscopic study of the action of uranyl acetate on the erythrocyte at varying molarity and tonicity
    (Australian Atomic Energy Commission, 1977-03) Wyatt, JH
    Phase contrast and dark field microphotographs were made to record variation of the shape and size changes seen when human erythrocytes are exposed in a number of ways to uranyl acetate in vitro. The degree of hemolysis produced by varying the tonicity of the uranyl acetate solutions was measured, and the results are discussed with particular reference to the possible influence of pH.
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    Ultrastructure changes produced by the action of uranyl acetate on the human erythrocyte in vitro
    (Australian Atomic Energy Commission, 1975-06) Wyatt, JH
    Human erythrocytes exposed in vitro to low concentrations of uranyl ions are immediately changed in shape to stomatocytes. Electron microscope examination demonstrates that cellular damage is confined to the plasma membrane. Endocytosis of the cell membrane produces groups of inside out membrane-lined vesicles within the cell; lipid from the membrane enters the cell, giving rise to intracellular myelin figures, and breaks are seen in the cell membrane. The degree and type of change is shown to be a dose-dependent phenomenon. It is proposed that the lipid fraction of the cell membrane is the primary target for damage by uranyl ions.
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    Vascular injury in lung disease
    (Australian Atomic Energy Commission, 1975) Tucker, AD; Wyatt, JH; Barry, JM; Undery, D
    Inhaled particulates which stimulate a 'delayed', cellular mode of alveolar clearance are excreted to the airways through lymphoid foci in the bronchial bifurcations. The anatomic relations and developing pathology of the tissues adjacent to these foci, including the divisions of accompanying arteries, were studied by serial sectioning and photo-micrographic modelling of rat lungs. The changes are typical of classic 'delayed' inflammatory reactions and, in the rat, the fully developed stage is characterised by fibrinoid necrosis involving all three layers of the arterial wall in a linear lesion across the leading edge of the flow divider. An hypothesis was developed to relate the injury to pulsatile forces. Recent published findings indicate that similarly placed lesions, with species-specific changes in development, are universal in both cerebral and extra-cranial arterial forks of man and animals. Possible associations of the microvascular changes with human atherosclerosis and their further significance in pulmonary and systemic effects arising from industrial and environmental contaminants are explored.