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The morfoestructural changes that appear at renal tubule level in obstructive uropathy consist in a progressive loss of the differentiations in the plasmatic membrane: reduction in the number of apical microvilli and of basal invaginations, which entails a drop in the exchange surface area. Degeneration and cellular necrosis phenomena also exist, with the appearance of cell traces in the tubule lumen. On the other hand, morphological signs of a rapid rate of cellular activity in the tubule cells are displayed. Together with the modifications that take place at basal membrane level these changes give rise to an alteration of tubule dynamics.
In experimental obstructive uropathy the renal interstice undergoes profound modifications, from the earliest stages, with the fibroblastic elements adopting a palisade arrangement between the renal tubules and the blood cells. Between these cells there is a marked edema configuring "canals", which could be the morphological image of the tubulovenous reflux described in obstructive uropathy. these routes, which we will call tubule-interstice-vein "canals", since in no case could we verify the existence of a direct communication between the tubule formations and the veins, disappear in animals put down late, where fibro and myofibroblastic elements, round cells and macrophages proliferate. A larger number of fibres and fundamental substance are also found. As a result of these changes, a great alteration in renal architecture takes place.
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The experiments on the model of altitude-chamber hypoxia in rats have established that within 15 days the secretory activity of terminal bronchiolar Clara cells increased in the secret accumulation phase and was accompanied by the transformation of the apical surface relief and ultrastructure of synthetic cell apparatus. Chronic hypoxia lasting for up to 60 days leads to compensation-adaptation changes of Clara cell ultrastructure, providing the intensification of secretion processes and postsecretion repair of membranes of the apical surface cells.
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Candida albicans yeast cells were treated prior to their growth phase with isoconazole at the following concentrations: 0.1 microgram/ml, 1 microgram/ml, 10 micrograms/ml), isoconazole induces a blockade of cell diprecipitates bearing witness to the presence of polysaccharides were noted in the cytoplasma and against the membrane wall, but cell division was apparently unaffected. At low concentrations (1 microgram/ml, 10 microgram/ml), isoconazole induced a blockade of cell division by its fungicidal action on synthesis and organisation of the membrane wall. At higher concentrations (50 microgram/ml; 100 micrograms/ml), isoconazole induces total necrosis and death. These findings confirm the analogy between the fungicidal actions of isoconazole and miconazole; however, the site of action of imidazole derivatives (wall or plasma membrane) is discussed.
A new continuous retinoblastoma cell line (Rb 355-7) derived from a nonfamilial unilaterally-affected child was studied morphologically and with regard to HLA expression. The tumor was compared with two older and widely studied cell lines, the Y-79 and WERI-Rb1 strains. The Rb 355-7 line grew in tissue culture in clusters and chains. Its doubling time was calculated to be 4.4 days. In contrast to the Y-79 and WERI-Rb1 cell lines, the Rb 355-7 showed a paucity of HLA expression.
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