Non-equilibrium phase transitions in biomolecular signal transduction

We study a mechanism for reliable switching in biomolecular signal-transduction cascades. Steady bistable states are created by system-size cooperative effects in populations of proteins, in spite of the fact that the phosphorylation-state transitions of any molecule, by means of which the switch is implemented, are highly stochastic. The emergence of switching is a nonequilibrium phase transition in an energetically driven, dissipative system described by a master equation. We use operator and functional integral methods from reaction-diffusion theory to solve for the phase structure, noise spectrum, and escape trajectories and first-passage times of a class of minimal models of switches, showing how all critical properties for switch behavior can be computed within a unified framework

Counting inequivalent monotone Boolean functions

Monotone Boolean functions (MBFs) are Boolean functions $f: {0,1}^n \rightarrow {0,1}$ satisfying the monotonicity condition $x \leq y \Rightarrow f(x) \leq f(y)$ for any $x,y \in {0,1}^n$. The number of MBFs in n variables is known as the $n$th Dedekind number. It is a longstanding computational challenge to determine these numbers exactly - these values are only known for $n$ at most 8. Two monotone Boolean functions are inequivalent if one can be obtained from the other by renaming the variables. The number of inequivalent MBFs in $n$ variables was known only for up to $n = 6$. In this paper we propose a strategy to count inequivalent MBF's by breaking the calculation into parts based on the profiles of these functions. As a result we are able to compute the number of inequivalent MBFs in 7 variables. The number obtained is 490013148

Leader Election in Anonymous Rings: Franklin Goes Probabilistic

We present a probabilistic leader election algorithm for anonymous, bidirectional, asynchronous rings. It is based on an algorithm from Franklin, augmented with random identity selection, hop counters to detect identity clashes, and round numbers modulo 2. As a result, the algorithm is finite-state, so that various model checking techniques can be employed to verify its correctness, that is, eventually a unique leader is elected with probability one. We also sketch a formal correctness proof of the algorithm for rings with arbitrary size

Distributed (Δ+1)(\Delta+1)-Coloring in Sublogarithmic Rounds

We give a new randomized distributed algorithm for $(\Delta+1)$-coloring in the LOCAL model, running in $O(\sqrt{\log \Delta})+ 2^{O(\sqrt{\log \log n})}$ rounds in a graph of maximum degree~$\Delta$. This implies that the $(\Delta+1)$-coloring problem is easier than the maximal independent set problem and the maximal matching problem, due to their lower bounds of $\Omega \left( \min \left( \sqrt{\frac{\log n}{\log \log n}}, \frac{\log \Delta}{\log \log \Delta} \right) \right)$ by Kuhn, Moscibroda, and Wattenhofer [PODC'04]. Our algorithm also extends to list-coloring where the palette of each node contains $\Delta+1$ colors. We extend the set of distributed symmetry-breaking techniques by performing a decomposition of graphs into dense and sparse parts

Categorical Ontology of Complex Systems, Meta-Systems and Theory of Levels: The Emergence of Life, Human Consciousness and Society

Single cell interactomics in simpler organisms, as well as somatic cell interactomics in multicellular organisms, involve biomolecular interactions in complex signalling pathways that were recently represented in modular terms by quantum automata with ‘reversible behavior’ representing normal cell cycling and division. Other implications of such quantum automata, modular modeling of signaling pathways and cell differentiation during development are in the fields of neural plasticity and brain development leading to quantum-weave dynamic patterns and specific molecular processes underlying extensive memory, learning, anticipation mechanisms and the emergence of human consciousness during the early brain development in children. Cell interactomics is here represented for the first time as a mixture of ‘classical’ states that determine molecular dynamics subject to Boltzmann statistics and ‘steady-state’, metabolic (multi-stable) manifolds, together with ‘configuration’ spaces of metastable quantum states emerging from complex quantum dynamics of interacting networks of biomolecules, such as proteins and nucleic acids that are now collectively defined as quantum interactomics. On the other hand, the time dependent evolution over several generations of cancer cells --that are generally known to undergo frequent and extensive genetic mutations and, indeed, suffer genomic transformations at the chromosome level (such as extensive chromosomal aberrations found in many colon cancers)-- cannot be correctly represented in the ‘standard’ terms of quantum automaton modules, as the normal somatic cells can. This significant difference at the cancer cell genomic level is therefore reflected in major changes in cancer cell interactomics often from one cancer cell ‘cycle’ to the next, and thus it requires substantial changes in the modeling strategies, mathematical tools and experimental designs aimed at understanding cancer mechanisms. Novel solutions to this important problem in carcinogenesis are proposed and experimental validation procedures are suggested. From a medical research and clinical standpoint, this approach has important consequences for addressing and preventing the development of cancer resistance to medical therapy in ongoing clinical trials involving stage III cancer patients, as well as improving the designs of future clinical trials for cancer treatments.\ud \ud \ud KEYWORDS: Emergence of Life and Human Consciousness;\ud Proteomics; Artificial Intelligence; Complex Systems Dynamics; Quantum Automata models and Quantum Interactomics; quantum-weave dynamic patterns underlying human consciousness; specific molecular processes underlying extensive memory, learning, anticipation mechanisms and human consciousness; emergence of human consciousness during the early brain development in children; Cancer cell ‘cycling’; interacting networks of proteins and nucleic acids; genetic mutations and chromosomal aberrations in cancers, such as colon cancer; development of cancer resistance to therapy; ongoing clinical trials involving stage III cancer patients’ possible improvements of the designs for future clinical trials and cancer treatments. \ud \u