DYNAMIC PATTERN IN CHEMICALLY REACTING SYSTEMS

这项研究的长期目标是进一步 理解相互作用的聚合物的动力学行为 细胞，并将这些知识应用于细胞运动和 发育生物学中的模式形成和生理学中的问题。 本研究福尔斯分为四大类：（1）模式研究 发育中的形成，（2）趋化性研究，（3） 兴奋系统;（4）心脏动力学研究。第（1）项下的目标 是开发和分析细胞粘液中丘形成的模型 霉菌Dictyosteoblastedeum，其结合了起搏器，cAMP生产 扩散、细胞间相互作用、细胞分化和细胞 分类（2）的目的是开发和分析细菌的模型， 适应和做三维聚集的模拟 浓度场（3）的主要目的是研究 卵母细胞钙通道动力学的研究 不同类型的钙通道对刺激反应的影响 波的特性和传播。第（4）项下的目标是（I） 开发一个钙动力学和细胞膜的综合模型， 心肌细胞中的电位，以了解自发钙 释放，和（ii）研究各向异性的成因中的作用， 心室组织纤维性颤动。 本研究（1）和（2）部分的结果将推动我们的研究。 了解发育生物学中的几个基本过程：信号 转导，细胞-细胞信号传导，细胞和组织运动和空间 图案形成更好地理解这些过程将 有助于更好地了解系统如何应对其 环境，正常的发展如何被破坏，以及如何确定 免疫系统的功能。的工作成果 （3）和（4）中描述的将进一步理解其中一个 美国主要的公共卫生问题，心脏性猝死， 每天约1000人。大多数是由快速不规则的 心律称为心室颤动，通常由 室性心动过速拟议工作的结果将有助于 对我们理解宇宙起源的两个重要方面 心律不齐首先，单细胞模型， 关于膜动力学和钙处理的知识将促进我们的 了解这些组件如何相互作用以及这种相互作用 可局部产生室性心动过速。第二，整合 将单细胞动力学转化为大规模的心脏组织模型， 提供了如何抑制异常的局部行为的洞察力， 与邻近组织的相互作用， 异常是为了产生大规模（组织范围）的破坏， 传播，以及超临界局部异常如何随时间演变。一 更好地理解可能导致 室性心动过速及其如何演变为 心室颤动可能导致抑制它们的新策略 从而对公众健康产生重要影响。

The long range objectives of this research are to further the understanding of the dynamical behavior of aggregates of interacting cells, and to apply this knowledge to problems of cell movement and pattern formation in developmental biology and to problems in physiology. The research falls into four major categories: (1) studies on pattern formation in development, (2) studies on chemotaxis, (3) studies on excitable systems, and (4) studies on cardiac dynamics. The aim under (1) is to develop and analyze models for mound formation in the cellular slime mold Dictyostelium discideum that incorporate pacemakers, cAMP production and diffusion, cell-cell interactions, cell differentiation and cell sorting. The aim in (2) is to develop and analyze a model for bacterial adaptation and to do simulations of aggregation in three-dimensional concentration fields. The major objective in (3) is to study models of calcium channel dynamics in oocytes with a view toward understanding the effect of different types of calcium channels on the stimulus-response characteristics and the propagation of waves. The aims under (4) are (I) to develop an integrated model for calcium dynamics and the membrane potential in cardiac myocytes in order to understand spontaneous calcium release, and (ii) to study the role of anisotropy in the genesis of fibrillation in ventricular tissue. The results of parts (l) and (2) of this research will advance our understanding of several basic processes in developmental biology: signal transduction, cell-cell signaling, cell and tissue motion and spatial pattern formation. A better understanding of these processes will contribute to a better understanding of how systems respond to their environment, how normal development can be disrupted, and how certain components of the immune system function. The results of the work described under (3) and (4) will further our understanding of one of the major public health problems in the US, sudden cardiac death, which claims approximately 1000 individuals per day. Most result from a rapid irregular rhythm called ventricular fibrillation, which often evolves from ventricular tachycardia. The results of the proposed work will contribute to our understanding of two important aspects of the genesis of arrhythmias. Firstly, single-cell models that incorporate current knowledge about membrane dynamics and calcium handling will advance our understanding of how these components interact and how this interaction can produce ventricular tachycardia locally. Secondly, integrating the single-cell dynamics into a large-scale model of cardiac tissue will provide insight into how aberrant local behavior can be suppressed by interaction with neighboring tissue, what the critical space scale of abnormality is for production of large-scale (tissue-wide) disruption of propagation, and how supercritical local abnormalities evolve in time. A better understanding of the different mechanisms that can give rise to ventricular tachycardia and an understanding of how it evolves into ventricular fibrillation may lead to new strategies for suppressing them and thereby have an important impact on public health.