The dynamics of quantifiable homeostasis. III: a linear model of certain metrical diseases.
The dynamics of quantifiable homeostasis. III: a linear model of certain metrical diseases.
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可量化的动态平衡。
DOI：
10.1002/ajmg.1320180106
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
E. Murphy
中科院分区：
文献类型：
--
作者：
W. A. Renie;E. Murphy
线性、滞后、稳态过程的推广表明，性状函数的位移是否随时间消失，是否无限地持续，或是否表现出稳定放大的（野生的）振荡，取决于滞后时间和恢复常数的乘积所假定的值。此外，它示出，如果使用一个稳定的位移力，而不是一个瞬时位移，一个新的归位值的结果是由位移力的恢复系数的比率。结合这两个发展，为确定停药时是否会发生过冲（例如，停用肝素后的反跳性血栓形成）提供了依据。这些想法的进一步发展表明，在成熟患者中开始的糖尿病如何可以完全由该疾病中发生的胰岛素反应滞后的众所周知的延长来解释。如果要在滞后时间增加时避免剧烈振荡，则必须减弱恢复常数（显然是通过胰岛素受体的系统性减少），而这种减弱意味着归巢值被取代。因此，这种糖尿病中的高血糖症被视为为避免剧烈振荡而付出的代价。如果外源性胰岛素的治疗应用是系统的和规律的，而不是控制论的，那么它在内源性（控制论）胰岛素分泌失败的情况下的成功是容易理解的。这一点可以通过一个熟悉的类比来说明，即一个反应缓慢的汽车司机。这些想法的遗传和进化的影响进行了概述。
A generalization of the linear, lagged, homeostatic process shows that whether a displacement of the trait function dies out with time, continues indefinitely, or shows a steadily amplifying (wild) oscillation depends on the value assumed by the product of the lag time and the restoration constant. Moreover, it is shown that if a steady displacing force is used rather than an instantaneous displacement, a new homing value results which is given by the ratio of the displacing force to the restoration coefficient. Combining these two developments furnishes grounds for determining whether or not an overshoot will occur when administration of a drug is stopped (for instance, the rebound thrombosis on discontinuing heparin). Further developments of these ideas show how the diabetes that begins in mature patients can be wholly accounted for by the well-known prolongation of the lag in insulin response that occurs in that disorder. If wild oscillation is to be avoided as the lag time increases, the restoration constant must be weakened (evidently by a systematic reduction in insulin receptors) and this weakening means that the homing value is displaced. Thus the hyperglycemia in this diabetes is to be seen as the price paid for avoiding wild oscillation. Provided that the therapeutic use of exogenous insulin is systematic and regular, rather than cybernetic, its success where endogenous (cybernetic) insulin secretion has failed is readily understood. The point is illustrated by a familiar analogy of a car driver with slow responses. The genetic and evolutionary implications of these ideas are outlined.