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肌球小体病病因的实验研究

Experimental study of the cause of myospherulosis.

作者信息

Kakizaki H, Shimada K

机构信息

Department of Morphological Pathology, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan.

出版信息

Am J Clin Pathol. 1993 Mar;99(3):249-56. doi: 10.1093/ajcp/99.3.249.

Abstract

To elucidate the nature of myospherulosis, the authors tried to produce this state in vitro by mixing vitamin E, oleic acid, linoleic acid, and lanolin with human blood components, such as whole blood, washed erythrocytes, plasma, and fixed erythrocytes, respectively. Myospherulosis was produced in all mixtures in these experiments. The authors concluded the following. A thin parent body wall of myospherulosis is formed initially as a result of the physical emulsion phenomenon between lipid-containing materials and blood. Erythrocytes then are enclosed in the parent body. The parent body membrane gradually is reinforced by the deposition of plasma proteins, which are insoluble in ethanol. Thereafter, the erythrocytes become endobodies by the deposition of their contents to the membrane of the parent body. The pores of the endobodies are formed in the process of erythrocyte degeneration. The contents of the erythrocytes, such as hemoglobin, would attach to the parent body. Thus myospherulosis would become complete. In humans, the characteristics of the parent body membranes differ from each other, depending on how much the hemoglobin or a part of the endobody membrane attaches to the parent body membrane.

摘要

为阐明类肌球形体病的本质,作者分别将维生素E、油酸、亚油酸和羊毛脂与人体血液成分(如全血、洗涤红细胞、血浆和固定红细胞)混合,试图在体外产生这种状态。在这些实验中,所有混合物均产生了类肌球形体病。作者得出以下结论。类肌球形体病的薄母体壁最初是由于含脂质物质与血液之间的物理乳化现象形成的。然后红细胞被包裹在母体内。母体膜通过不溶于乙醇的血浆蛋白沉积逐渐得到强化。此后,红细胞通过其内容物沉积到母体膜上而成为内体。内体的孔隙在红细胞变性过程中形成。红细胞的内容物,如血红蛋白,会附着在母体上。这样类肌球形体病就形成了。在人类中,母体膜的特征彼此不同,这取决于血红蛋白或内体膜的一部分与母体膜附着的程度。

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