Angular homeostasis II: Pursuit of a moving target in a plane and some implications for cardiac teratology.
Angular homeostasis II: Pursuit of a moving target in a plane and some implications for cardiac teratology.
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角稳态 II：平面上移动目标的追踪以及对心脏畸形学的一些影响。
DOI：
10.1002/ajmg.1320310219
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Murphy,EA
中科院分区：
文献类型：
--
作者：
Sagawa,Y;Berger,KR;Trojak,JE;Brown,KL;Murphy,EA
分析了心脏个体发生的一种模型。它是通过同一平面上的一系列细胞的生长来追逐线性移动的目标的几何形式，追踪者在每一步都朝着目标的当前位置调整其生长方向。终点是它们之间的融合，它可以以两种方式发生：要么通过追赶者的领先细胞追赶目标(追赶者介导的融合，或PMF)，要么通过目标跑到追赶者的预成一侧(靶介导的融合，或TMF)。因果规格是步长、追踪者的速度、目标的速度、恢复常数和追赶者的初始方向；结果变量是融合的步数和融合模式。行为模式是复杂的，在大片价值观上或多或少是有规律的，穿插着突然的、门槛般的变化，可能会产生一种二分的遗传模式，尽管其他原因的遗传因素不断递增。暂时取消矫正过程(这一改变是为了模拟致畸因素的影响模式而引入的)可能会推迟融合，并可能暗示隔膜如何无法融合，动脉导管如何关闭，或如何形成心内膜垫。但该模型还预测，在某些看似合理的条件下，“畸胎原”会加速融合，从而可能抵消先天缺陷的遗传易感性。
A model of cardiac ontogenesis is analyzed. It is cast in terms of the geometry of the pursuit of a linearly movingtargetby the growth of a chain of cells in the same plane, thepursuer, which at each step adjusts its direction of growth towards the current position of the target. The endpoint is the fusion between them, which can occur in 2modes: either by the leading cell of the pursuer catching up with the target (pursuer‐mediated fusion, orPMF) or by the target running into the preformed side of the pursuer (target‐mediated fusion, orTMF). The causal specifications are the step size, the speed of the pursuer, the speed of the target, the restoration constant, and the initial direction of the pursuer; the outcome variables are the number of steps to fusion and the mode of fusion. The pattern of behavior is complicated, being more‐or‐less regular over large tracts of values, interspersed with abrupt, threshold‐like changes that may generate a dichotomous pattern of inheritance despite a continuous gradation of genetic of other causes. The temporary abolition of the correction process (a change introduced to simulate the pattern of the effect of a teratogen) may delay fusion and suggest how a septum may fail to fuse, the ductus arteriosus to close, or an endocardial cushion to form. But the model also predicts that under certain plausible conditions, the “teratogen” would speed up fusion and hence perhaps offset a genetic predisposition to a congenital defect.