[Diameter and arrangement of enamel prisms. A morphological study].
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Biomedical subjects
Publications and source records attributed to G Steding.
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Developmental disorders in the period of the differentiation of the primitive foregut leads to atresia of the esophagus with tracheoesophageal fistula. Most authors think that this differentiation is caused by lateral foregut folds, which fuse in midline, thus forming the tracheoesophageal septum. In order to gain information about this period of development, we studied the foregut region of chick embryos by scanning electron microscopy (SEM) and light microscopy. In our study no signs of lateral folds or fusing foregut wall components, which were forming a tracheoesophageal septum, were found. Our study suggests that the development of the esophagus and trachea is the result of a simple reduction of the size of the primitive foregut. The consequence for the understanding of the embryology of the foregut malformations is discussed.
Different regions of broken enamel of human permanent teeth are observed by means of a scanning electron microscope. The diameter of the prisms must be considered as constant from the dentino-enamel junction up to the enamel surface.
A concept for the explanation of the formal genesis of congenital cardiac malformations is introduced, based on the observation that 1. the septa in the outflow-tract of the heart are formed in spatial relation to changes in form of the external cardiac wall and always along the longer sides of the ovally deformed pathway of flow, 2. the muscular septa (ventricular and atrial septa) arise as protrusions due to different directions of ventricular growth. Accordingly, no septa develop when normal deformation fails to occur (e.g. truncus communis); septa are incompletely developed when the deformation is insufficient (e.g. aortico-pulmonary window); septa are formed in wrong positions where the direction of deformation deviates more or less from the normal direction (as in stenosis due to slight deviation, or transposition due to large deviation from the normal). The so-called ventricular inversions and atrio-ventricular discordance are regarded as consequences of dystopic development of the ventricular septum. This concept for the explanation of the formal genesis of cardiac malformations is exemplified by variants of transpositions (anatomically corrected and uncorrected), and by variants of double-outlet-right-ventricle and double-outlet-left-ventricle. Using a common anomaly (tetralogy of Fallot) and 2 rare ones (double-outlet-right-ventricle with complete AV canal, and criss-cross-heart) it is shown that the interpretation of the development of cardiac malformations as a consequence of dystopic development of the septa allows an understanding of the formal genesis of complex malformations without involving hitherto unproven developmental processes.
The present paper reports our study of the developmental transformation of the aortic arch complex. A system of interarterial septa in the region of the embryonic aortic arch complex is demonstrated by means of microdissection and scanning electron microscopy. Local differences in growth of the dorsal and ventral free edges of these interarterial septa define, together with the commonly known obliteration of arterial segments, the arrangement of the origin of the great arteries. On the basis of this interarterial septal system a concept of disturbed interarterial septal growth, complemental to the long-established mechanism of obliteration, is introduced for interpretation of the formal genesis of malformations of the great arteries and their branches arising from the heart. The following pathogenetic mechanisms are suggested to contribute to the development of malformations in the aortic arch complex: 1. Increase or decrease of the number of interarterial septa 2. Excessive or reduced septal growth or deviating growth directions 3. Origin of septa in abnormal positions 4. Abnormal blending of the free edges of interarterial septa 5. Abnormal connection with the truncus septa 6. Abnormal processes of obliteration.
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The formation of the relief of cardiac septa occurs in connexion with the development of shape of the external cardiac wall. Changes in the form of the external cardiac wall precede changes in the internal cardiac wall. The originally straight tubular heart is angulated at typical sites during cardiac looping. At the site of angulations the primary circular cross-section is deformed to an oval and is thereby narrowed. This deformation causes a growth of the endocardial and subendocardial tissue along the long sides of the oval to form protrusions into the cardiac lumen. These protrusions represent the anlagen of the fibrous cardiac septa. The site of origin of the fibrous septa is directly dependent on the direction of primary deformation. Origin and site of the ventricular septum results from the locally different directions and patterns of growth in the right and left ventricle. The anlagen of the cardiac septa are not isolated formations, but rather represent a continuous system of protrusions. Depending on the position and form of its components, their free edges grow towards each other and fuse wherever they meet.
Morphogenetic movements of the anterior intestinal port of in vitro growing chick embryos were recorded in stages 5--12 by means of microkinematography. Anterior intestinal port moves between stages 7 and 12 by 1.02 mm caudally, while the cranial end of the head migrates by 0.45 mm cranially. Rate of descensus, which is high during stages 7--9, decreases continually, approaching 0 in stage 12. The results are discussed in connection with the formation of intestinal port and of foregut.
The levo-atrial systemic vein is a special type of persistent left superior vena cava and is associated with other intracardiac lesions most often. Hemodynamically there is a right to left shunt. The operative procedure may consist in a ligature in relation to the anatomic situation. The intraatrial correction intends a drainage to the right atrium. Of 7 cases four times a intracardiac rerouting was achieved but two times a ligation was performed.
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