Cells of multicellular organisms communicate with each other through gap junctions composed of connexin proteins. The totality of gap junction communication among a group of cells is a Gap Junction Bioelectric Network (GJBN). Even though the rule governing a GJBN may be simple, its computations can be complex.
The Principle of Computational Equivalence (PCE) holds that Wolfram cellular automaton #110 is sufficiently complex to model the computations of a complex GJBN. The Principle of Computational Irreducibility (PCI) maintains that a complex GJBN cannot be modeled accurately and comprehensively by 'shortcut' equations. Instead, the system must be 'run' to observe its outcome.
It is proposed that aging and cancer are the result of chronic entropic dysregulation of the complex asymmetric GJBN modeled by cellular automaton #110 into a symmetric random network modeled by cellular automaton #30. Consequently, asymmetric morphogen gradients necessary for the geometric stability of the organism (morphostasis) are gradually lost, and the organism 'grows' old and develops cancer. The Hayflick limit, shortening of telomeres, and telomerase activity are not the proximate causes of aging and cancer.
Successful cancer prevention/treatment, and anti-aging or rejuvenation strategies will require a systems approach that maintains or restores the complex GJBN modeled by Wolfram cellular automaton #110.
Inhaltsverzeichnis (Table of Contents)
- Introduction
- Main Part
- Discussion
- Summary
- References
Zielsetzung und Themenschwerpunkte (Objectives and Key Themes)
This paper proposes that computations of the Gap Junction Bioelectric Network (GJBN) can be modeled by cellular automata, specifically Wolfram cellular automaton #110. The paper argues that entropic dysregulation of this complex GJBN is a key factor in the processes of aging and cancer.
- Modeling the GJBN with cellular automata
- The role of entropic dysregulation in aging and cancer
- The limitations of differential equations in capturing the complexity of biological systems
- The importance of the Principle of Computational Equivalence (PCE) and the Principle of Computational Irreducibility (PCI) in understanding GJBN*110
- The scale-free, fractal structure of a multicellular organism as a Gap Junction Bioelectric Network (GJBN*110)
Zusammenfassung der Kapitel (Chapter Summaries)
- Introduction: This chapter introduces the concept of a Gap Junction Bioelectric Network (GJBN) and its potential for modeling with cellular automata. It highlights the importance of Wolfram cellular automaton #110 as a complex system capable of representing the GJBN. The chapter discusses the limitations of differential equations in capturing the complexity of biological systems and emphasizes the need for models based on GJBN*110.
- Main Part: This chapter delves into the detailed analysis of GJBN*110. It describes how gap junction movements of negatively-charged chloride ions influence cell membrane potential (Vmem) and Vmem gradients. It explains the role of morphogens in activating genes and gap junction conductivities, and discusses the relationship between Vmem gradients and morphogen gradients. The chapter emphasizes the importance of GJBN*110 in understanding the complexities of embryogenesis, morphogenesis, aging, and cancer.
Schlüsselwörter (Keywords)
Gap Junction Bioelectric Network (GJBN), cellular automaton, Wolfram cellular automaton #110, entropic dysregulation, aging, cancer, Principle of Computational Equivalence (PCE), Principle of Computational Irreducibility (PCI), scale-free network, fractal structure, morphogen, cell membrane potential (Vmem), embryogenesis, morphogenesis.
- Citation du texte
- MD Dr. Marshall Goldberg (Auteur), 2018, The cellular automaton interpretation of aging and cancer, Munich, GRIN Verlag, https://www.grin.com/document/425564
