## BACKGROUND. Cardiotoxicity, including ischemia and myocardial infarction, is one of the complications observed after treatment with interferon (IFN). Therefore, the question has been raised whether IFN may cause damage to the small myocardial blood vessels. ## METHODS. In this study, 400 U o
An ultrastructural study of lens invagination in the mouse
โ Scribed by Wrenn, Joan T. ;Wessells, Norman K.
- Publisher
- John Wiley and Sons
- Year
- 1969
- Tongue
- English
- Weight
- 915 KB
- Volume
- 171
- Category
- Article
- ISSN
- 0022-104X
No coin nor oath required. For personal study only.
โฆ Synopsis
Early lenses of mouse embryos were studied with the electron microscope to determine whether their cells contain organelles that can be causally related to the invagination of the lens placode. The cells of the placode and early lens cup are joined at their apical ends by junctional complexes. At the level of the zonula adhaerens, favorabIe sections show cytoplasmic filaments, 35 A to 50 A wide, arranged about the apex of a cell. Groups of filaments appear to originate on or near the plasma membrane and then to extend across the cytoplasm, parallel to the apical cell surface, to terminate on or near the plasma membrane some distance away. They are nearly always straight; in contrast, nearby lateral and apical cell membranes are twisted into irregular folds and projections.
We present a model to explain lens invagination in which the filaments are considered to be contractile. On the basis of their location in the cells and their presumed function, these organelles are proposed to be a major component in the mechanism that leads to early morphogenesis of the lens.
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Adult homozygous lap mice show various eye abnormalities, such as aphakia, retinal disorganization, and dysplasia of the cornea and anterior chamber. In the fetal eye of a homozygous lap mouse, the lens placode seems to develop normally. However, the lens vesicle progresses abnormally to form a mass
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