In a diffusion-based molecular communication network, transmitters and receivers communicate by using signalling molecules (or ligands) in a fluid medium. This paper assumes that the transmitter uses different chemical reactions to generate different emission patterns of signalling molecules to represent different transmission symbols, and the receiver consists of receptors. When the signalling molecules arrive at the receiver, they may react with the receptors to form ligand-receptor complexes. Our goal is to study the demodulation in this setup assuming that the transmitter and receiver are synchronised. We derive an optimal demodulator using the continuous history of the number of complexes at the receiver as the input to the demodulator. We do that by first deriving a communication model which includes the chemical reactions in the transmitter, diffusion in the transmission medium and the ligand-receptor process in the receiver. This model, which takes the form of a continuous-time Markov process, captures the noise in the receiver signal due to the stochastic nature of chemical reactions and diffusion. We then adopt a maximum a posteriori framework and use Bayesian filtering to derive the optimal demodulator. We use numerical examples to illustrate the properties of this optimal demodulator.
Models. This paper uses the Reaction Diffusion Master Equation (RDME) @cite_38 framework to model the reactions and diffusion in the molecular communication networks. RDME assumes that time is continuous while the diffusion medium is discretised into voxels. This results in a CTMP with finite number of (discrete) states. RDME has been used to model stochastic dynamics of cells in the biology literature @cite_8 . An attraction of RDME is that it has the Markov property which means that one can leverage the rich theory behind Markov process.
@cite_38 @cite_8
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We outline our perspective on stochastic chemical kinetics, paying particular attention to numerical simulation algorithms. We first focus on dilute, well-mixed systems, whose description using ordinary differential equations has served as the basis for traditional chemical kinetics for the past 150 years. For such systems, we review the physical and mathematical rationale for a discrete-stochastic approach, and for the approximations that need to be made in order to regain the traditional continuous-deterministic description. We next take note of some of the more promising strategies for dealing stochastically with stiff systems, rare events, and sensitivity analysis. Finally, we review some recent efforts to adapt and extend the discrete-stochastic approach to systems that are not well-mixed. In that currently developing area, we focus mainly on the strategy of subdividing the system into well-mixed subvolumes, and then simulating diffusional transfers of reactant molecules between adjacent subvolumes together with chemical reactions inside the subvolumes. Although cell polarity is an essential feature of living cells, it is far from being well-understood. Using a combination of computational modeling and biological experiments we closely examine an important prototype of cell polarity: the pheromone-induced formation of the yeast polarisome. Focusing on the role of noise and spatial heterogeneity, we develop and investigate two mechanistic spatial models of polarisome formation, one deterministic and the other stochastic, and compare the contrasting predictions of these two models against experimental phenotypes of wild-type and mutant cells. We find that the stochastic model can more robustly reproduce two fundamental characteristics observed in wild-type cells: a highly polarized phenotype via a mechanism that we refer to as spatial stochastic amplification, and the ability of the polarisome to track a moving pheromone input. Moreover, we find that only the stochastic model can simultaneously reproduce these characteristics of the wild-type phenotype and the multi-polarisome phenotype of a deletion mutant of the scaffolding protein Spa2. Significantly, our analysis also demonstrates that higher levels of stochastic noise results in increased robustness of polarization to parameter variation. Furthermore, our work suggests a novel role for a polarisome protein in the stabilization of actin cables. These findings elucidate the intricate role of spatial stochastic effects in cell polarity, giving support to a cellular model where noise and spatial heterogeneity combine to achieve robust biological function.