[Pharmaceutical studies on commercial phytonadion tablets and effect of polysorbate 80 on the dissolution test (author's transl)].
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Biomedical subjects
Publications and source records attributed to K Matsuba.
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Two penicillins and 5 cephalosporins were evaluated for their ability to pass through the outer-membranes of Proteus morganii, Citrobacter freundii and Escherichia coli. Cefazolin, ceftezole and cephaloridine showed high permeability through the outer-membranes of these Gram-negative bacteria. Benzylpenicillin and cephalothin, on the contrary, showed low permeability. The outer-membrane permeability of ampicillin and cephalexin varied from species to species. C. freundii was found to have the highest barrier against both the penicillins and the cephalosporins, and E. coli appeared to have a low barrier against the cephalosporins. The hydrophobic character of the beta-lactam antibiotics, which was estimated by a reversed-phase thin-layer chromatography was closely related to the outer-membrane permeability. In general, the more hydrophilic antibiotic showed the higher outer-membrane permeability. However, cephaloridine, the most lipophilic compound among the antibiotics tested, showed good permeability.
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In 101 patients with histopathologic and clinical features compatible with sarcoidosis, a radiologic acinar pattern occurred in about 20% and was always accompanied by bilateral hilar lymphadenopathy. The radiologically acinar pattern histopathologically revealed noncaseating epithelioid granulomas and accumulations of macrophages in the alveolar spaces. Blood vessels were usually not affected by granulomas. On the other hand, a reticulonodular pattern histopathologically showed granulomas with centrally situated veins. The acinar form seems to represent the early stage of pulmonary sarcoldosis, producing primarily intra-alveolar lesions.
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The number of conducting airways less than 2 mm in internal diameter was only slightly reduced in the lungs of 12 patients with pulmonary emphysema and diminished flow rates. There was a change in the distribution of the smallest remaining airways, with a deficit of airways 0.4 to 0.6 mm in diameter and an excess of airways smaller than this. The change in airway caliber and number was small in emphysematous lungs and increased airway resistance in emphysematous lungs is more likely related to loss of elastic recoil, central flow limitation and associated chronic bronchitis.
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