[A case of primary ciliary dyskinesia simulating diffuse panbronchiolitis].
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Biomedical subjects
Publications and source records attributed to F Kuze.
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The effects of epidermal growth factor (EGF) and transforming growth factor beta (TGF beta) on the growth of A431 epidermoid carcinoma cells were studied. Whereas the monolayer growth of A431 cells was inhibited by EGF, it was stimulated by TGF beta. Contrary to the effects on the monolayer growth, EGF stimulated the soft agar growth of A431 cells. The stimulatory effects of TGF beta on the anchorage-dependent growth were antagonized by EGF and those of EGF on anchorage-independent growth were antagonized by TGF beta. These results suggest that both factors not only convey the proliferative signals to A431 cells but also induce phenotypic changes, resulting in a preference for either anchorage-dependent or anchorage-independent growth. Moreover, as the stimulatory effects of EGF on the soft agar growth of A431 cells paralleled its reported stimulatory effects on their in vivo growth, it is also suggested that in vivo responses of cells to certain growth factors may correlate better with their responses in soft agar culture than with those in monolayer culture.
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Ultrastructure of the cell wall and peribacillary substances of various mycobacteria (32 strains of 18 species) grown in vitro was studied by a freeze-fracture technique. Peribacillary substances differed in shape among species and even among strains of the same species, and were classified into five types: (1) amorphous substances; (2) multi-layered sheaths with no filamentous units; (3) structures composed of filaments of 2-4 nm diameter, which were further classified into three subtypes according to the arrangement of the filaments; (4) helical fibres; and (5) single fibres, or networks of fibrous structures, with no visible substructures. No strains revealed peribacillary structures resembling those of uncultivable Mycobacterium leprae. These results have implications for the mechanism of freeze-fracturing in mycobacterial walls.
The effects of various chemotherapeutic regimens were investigated in ddY mice infected intravenously with a mouse-virulent strain, 31F093T, of Mycobacterium avium-intracellulare. Evaluation of therapeutic effects was based on serial counts of viable bacilli in the lung, the spleen, and the kidney, as well as on weight and extent of gross diseases of the organs, and on histopathologic examination. Kanamycin alone was effective against the infection. The combination of ethambutol and rifampin with kanamycin (KM-EMB-RMP) decreased counts in the lung. In another 3-drug regimen (kanamycin, ethionamide, and cycloserine), the effect was similar. Two 4-drug regimens, KM-EMB-RMP-CEX and KM-EMB-RMP-MINO, as well as a 5-drug regimen, KM-EMB-RMP-CS-INH, were also compared with the above 3-drug regimens, and only the 5-drug regimen decreased counts in the lung more than the 3-drug regimens did. Even the 5-drug regimen, however, could not eradicate the mycobacteria in the organs of mice, which demonstrates the inveteracy of M. avium-intracellulare infection. The control mice consistently showed grossly visible disease of the lung at 6 wk of infection, and the histopathologic findings were granuloma (3 to 6 wk of infection) and diffuse proliferative change beyond 9 weeks of infection, which was persistent and slowly progressive. The spleens and livers showed extensive granulomatous changes. The subacuteness of grossly visible lung disease with significant multiplication of bacilli in the organ of the control mice in the present murine model should prove useful in evaluating experimental chemotherapy of M. avium-intracellulare infection.