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    Architectural ultrastructure of the urinary bladder epithelium. II. Changes in the urine-blood barrier in the contracted and distended state in the normal and inflammatory bladder

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    1)正常群では, 表層細胞間結合部の機能的形態には, 標識物質の透過しないtight junctionと透過するleaky junctionの2種の構造がみられた.2)中間層および基底細胞間にはbarrierとしての機能的形態は存在しなかった.3)実験的炎症群では, leaky junctionは存在せず, 標識物質の透過は表層細胞の剥離した場合にのみ観察された.4)正常群および実験的炎症群において, 表層細胞間結合部のランタントレーサーに対する透過性は収縮および伸展により影響をうけなかった.5)膀胱移行上皮の尿・血液関門の1つに表層細胞間の接着装置複合体が考えられたThe urinary bladder epithelium in mammals, including humans, has a low permeability to ions and small molecules such as sodium, urea and water. Two structures, asymmetrical luminal plasma membrane and tight junction between superficial cells, have been said responsible for the urine-blood barrier. The permeability of junctional complex between superficial cells to lanthanum was observed in rat urinary bladder epithelium by transmission electron microscopy (TEM). In the normal bladder epithelium, confirmed by bacteriological examination, most junctions between superficial cells are the tight junctions and 1 to 9% of the junctions are leaky. The lanthanum, known to penetrate the leaky junctions, is demonstrated in the intercellular space between intermediate and basal cells. This suggests that desmosomes between these cells have no barrier function. In the experimentally inflammatory bladder epithelium all junctions are tight and no leaky junction is found between superficial cells. In contrast, if the superficial cells were stripped off in the inflammatory change, the lanthanum penetrates the junction between denuded intermediate cells. In the normal bladder epithelium the structural junctions between superficial cells have no changes during contraction and distension. Thus this suggests that the permeability to lanthanum does not change during contraction and distension

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    Usefulness of acceleration time ratio in diagnosis of internal carotid artery origin stenosis

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    獨協医科大学平成29年
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