Cell death in the morphogenesis and teratogenesis of the by Dr. méd. Tomas Pexieder (auth.)

By Dr. méd. Tomas Pexieder (auth.)

In spite of the ongoing development of study within the fields of mobile and molecular biology, which has orientated many embryologists in the direction of molecular biology, no concrete rationalization of morphogenesis has but been discovered. the current nation of data of center improvement is characterised by means of a tremendous discrepancy among the qualitative descriptions of what occurs at the organ point and the kind of quantitative details on subcellular and molecular occasions. it's quite often no longer understood how cells shape tissues and the way tissues generate specific types of an organ. In an try and fill the gaps we systematically studied within the interval 1968 to 1973 one of many basic yet relatively missed morphogenetic mechanisms which integrates cells into tissues and organs-cell dying. just a small a part of our learn on mobilephone dying within the improvement of chick, rat and human embryo hearts has as but been released in extenso. so much of it's been communicated in papers brought at varied clinical conferences. we want to exploit the chance provided via Advances to give a syn­ thesis and integrative evaluate of our effects. during this manner the particular interval of discovery of the life of cellphone loss of life and of its morphogenetic position within the center improvement come to an finish. This opens up the subsequent section of our learn which is composed in experiences of the way telephone dying is built-in with different morphogenetic mechanisms.

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Example text

The first positive results were obtained when the Nile blue sulphate stained pieces of heart bulbi were squashed (Saunders, 1966; Webster and Gross, 1970) in a drop of Ringer solution. In the case of nigrosin perfusion we could observe in the squash the absence of staining in healthy viable cells and a light diffuse staining of isolated dead cells. The most intense stain was observed in small dark grains on the surface of the macrophages. There was some faint diffuse staining in the phagosomes of the macrophages.

40 hours after the intervention (Fig. 50). The most spectacular changes were observed in the transition zone between the proximal right and distal ventral bulbar cushion (Figs. 40, 49 and 51). This zone, where in normal embryos cell death practically does not occur, was transformed as early as 16 hours after the experimental intervention into a new zone of intense cell death. The increase in the number of macrophages in this localization was significant also 40 and 48 hours post-operation. In all localizations but the proximal right bulbar cushion and the atrioventricular cushions the operative intervention continued to increase cell death intensity for the first 16 hours.

After the end of the staining period the right ventricle and the bulbus were incised under the dissecting microscope (Fig. 5). The stain which was mixed with some blood, was washed out by Ringer solution and the luminal surface of the bulbar cushions was inspected (Figs. 6, 8 and 24). We observed granular staining in regions revealed by hematoxylin-eosin stained serial sections (Figs. 1 % Nile blue sUlphate (Fluka) perfusions. The localization and the granular pattern of staining were identical in the case of these three stains.

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