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 clarification of morphogenesis has but been stumbled on. the current nation of data of middle improvement is characterised by way of a massive discrepancy among the qualitative descriptions of what occurs at the organ point and the roughly quantitative details on subcellular and molecular occasions. it really is often no longer understood how cells shape tissues and the way tissues generate specific different types of an organ. In an try to fill the gaps we systematically studied within the interval 1968 to 1973 one of many normal yet relatively ignored morphogenetic mechanisms which integrates cells into tissues and organs-cell loss of life. just a small a part of our learn on cellphone demise 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 added at diverse medical conferences. we want to exploit the chance provided via Advances to provide a syn­ thesis and integrative evaluate of our effects. during this manner the particular interval of discovery of the life of mobilephone loss of life and of its morphogenetic position within the center improvement come to an finish. This opens up the following section of our study which is composed in stories of ways phone loss of life is built-in with different morphogenetic mechanisms.

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Extra info for Cell death in the morphogenesis and teratogenesis of the heart

Sample text

During culture the heart fragments attached themselves to the filtre discs (Fig. 43) with some limited peripheral outgrowth. In the majority of cases the explants showed spontaneous contractions. Some supplementary degeneration was observed on the tissue-gas interface especially in the last part of the culture period (Fig. 44). Such degeneration was not considered in our calculations. A subsequent histological examination of some explants demonstrated a reduction in the amount of cardiac jelly (Figs.

78 and particle size 540-542 m[L (Stockinger, 1964). We have not found any paper discussing in sufficient detail the mechanism of vital staining with Nile blue sulphate. For this reason we are obliged to extrapolate from information about neutral red (Winckler, 1974). Mter penetration of the cell membrane and/or incorporation by endocytic processes these dyes initially stain the cytoplasm diffusely. , 1970; Winckler, 1974). It is now generally accepted that the particles of lysosomal character contain a glycolipid component in their matrix made strongly acidic by the presence of carboxyl or phosphate groups.

Q~~' <' : <:: ~ . ~'. Fig. 40. Influence of hemodynamic changes on the intensity and localization of cell death in the transition zone between the dista l ventral and proximal right bulbar cushions of the chick embryo heart. Schema of formal genesis of the ventricular septa l defect according to Rychter and Lemez (1959) pattern-and intelti;ity- changes we can see that an increase in cell death intensity precedes 8 to 16 h the morphologically identifiable reduction processes. This sequence of events was most striking in the case of the transition zone between the proximal right and distal ventral bulbar cushions (Fig.

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