By R. J. Kavlock, G. P. Daston (auth.), Robert J. Kavlock Ph.D., George P. Daston Ph.D. (eds.)
Having acquired the invitation from Springer-Verlag to provide a quantity on drug-induced delivery defects for the instruction manual of Experimental Pharmacology, we requested ourselves what new process may perhaps we provide that may seize the nation of the technological know-how and produce a brand new synthesis of the knowledge in this subject to the world's literature. We selected a three-pronged procedure, headquartered round these specific medicines for which we've a comparatively good confirmed foundation for realizing how they exert their negative effects at the human embryo. We then supplemented this data with a chain of reports of severe organic approaches thinking about the tested basic developmental styles, with emphasis on what occurs to the embryo whilst the techniques are perturbed through experimental capability. understanding that the quest for mechanisms in teratology has frequently been inhibited by way of the inability of knowing of the way general improvement proceeds, we additionally integrated chapters describing the fantastic new discoveries relating to the molecular keep watch over of standard morphogenesis for numerous organ platforms within the wish that the experimental toxicologists and molecular biologists will start to higher relish every one others questions and development. a number of occasions over the last years of constructing outlines, issuing invites, reviewing chapters, and cajoling belated individuals, we have now puzzled even if we made the proper determination to adopt this effort.
Read Online or Download Drug Toxicity in Embryonic Development I: Advances in Understanding Mechanisms of Birth Defects: Morphogenesis and Processes at Risk PDF
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Extra resources for Drug Toxicity in Embryonic Development I: Advances in Understanding Mechanisms of Birth Defects: Morphogenesis and Processes at Risk
BExpressed in both atrium and ventricle early, then one becomes dominant per segment. conotruncus, with weaker expression in the A V canal but none in the atrium or ventricles. Conversely, the myocardium of all segments expresses Csx-l and GATA-4 (LAVERRIERE et al. 1994). Similarly, all segments initially express both atrial and ventricular forms of myosin heavy chains, but, with time, their expression becomes restricted to the atrium or ventricle. , ventricular myosin light chain-2c (MLC-2c) or atrial myosin light chain-2a (MLC-2a), are entirely segmentally specific (WESSELS et al.
5). This junction between the ventricular segments has been termed the primary ring (WENINK 1987). Consistent with the concept of segmentation, the myocardial cells of the primary ring express tissue-specific antigens, such as GIN2 (WESSELS et al. 1991, 1992). The pattern of staining with anti-GIN2 antibodies and other markers is consistent with this ring being the site at which trabeculae fuse to form the muscular interventricular septum (LAMERS et al. 1992). Thus, while their morphogenetic roles may vary, the formation of muscular trabeculae or internal projections of quiescent or relatively slowly growing myocardium would seem to be a developmental fate common to atrial and ventricular segments (THOMPSON et al.
Three points are pertinent to the sequential formation of the cardiac segments by the fusion of the heart fields: (I) each has a different birthday and birthplace (position) within each heart field, (2) looping or bending of the heart tube accompanies the addition of segments, and (3) the segments have different developmental fates. , chambers arise by the interaction and remodeling of primitive segments. II. Morphology of the Primitive Segments As shown in Figs. 5 and 6, the wall of each primitive segment is lined by two concentric epithelia - the endocardium and myocardium - which initially blend seamlessly with those of adjacent segments.