搜索结果：signalling

Recent findings show that single, non-neuronal cells are also able to learn signalling responses developing cellular memory. In cellular learning nodes of signalling networks strengthen their interactions e.g. by the conformational memory of intrinsically disordered proteins, protein translocation, miRNAs, lncRNAs, chromatin memory and signalling cascades. This can be described by a generalized, unicellular Hebbian learning process, where those signalling connections, which participate in learning, become stronger. Here we review those scenarios, where cellular signalling is not only repeated in a few times (when learning occurs), but becomes too frequent, too large, or too complex and overloads the cell. This leads to desensitisation of signalling networks by decoupling signalling components, receptor internalization, and consequent downregulation. These molecular processes are examples of anti-Hebbian learning and forgetting of signalling networks. Stress can be perceived as signalling overload inducing the desensitisation of signalling pathways. Aging occurs by the summative effects of cumulative stress downregulating signalling. We propose that cellular learning desensitisation

The no-signalling principle is a fundamental assumption in Bell-inequality and quantum-steering experiments. Nonetheless, experimental imperfections can lead to apparent violations beyond those expected from finite-sample statistics. Here, we propose extensions of local hidden variable and local hidden state theories that allow for bounded, operationally quantifiable, amounts of signalling. We show how non-classicality tests can be developed for these models, both through exact methods based on the full set of observed statistics and through corrections to the standard Bell and steering inequalities. We demonstrate the applicability of these methods via two scenarios that feature apparent signalling: an IBM quantum processor and post-selected data from inefficient detectors.

We derive and simulate a mathematical model for mechanotransduction related to the Rho GTPase signalling pathway. The model addresses the bidirectional coupling between signalling processes and cell mechanics. A numerical method based on bulk-surface finite elements is proposed for the approximation of the coupled system of nonlinear reaction-diffusion equations, defined inside the cell and on the cell membrane, and the equations of elasticity. Our simulation results illustrate novel emergent features such as the strong dependence of the dynamics on cell shape, a threshold-like response to changes in substrate stiffness, and the fact that coupling mechanics and signalling can lead to the robustness of cell deformation to larger changes in substrate stiffness, ensuring mechanical homeostasis in agreement with experiments.

The causal effects activated by a quantum interaction are studied, modelling the last one as a bipartite unitary channel. The two parties, say Alice and Bob, can use the channel to exchange messages -- i.e. to signal. On the other hand, the most general form of causal influence includes also the possibility for Alice, via a local operation on her system, to modify Bob's correlations and viceversa. The presence or absence of these two effects are equivalent, but when they both occur, they can differ in their magnitude. We study the properties of two functions that quantify the amount of signalling and causal influence conveyed by an arbitrary unitary channel. The functions are proved to be continuous and monotonically increasing with respect to the tensor product of channels. Monotonicity is instead disproved in the case of sequential composition. Signalling and causal influence are analytically computed for the quantum SWAP and CNOT gates, in the single use scenario, in the $n$-parallel uses scenario, and in the asymptotic regime. A finite gap is found between signalling and causal influence for the quantum CNOT, thus proving the existence of extra causal effects that cannot be exp

Non-classical correlations resulting from entangled quantum systems have sparked debates about the compatibility of quantum theory and relativity, and about the right way to think about causation. Key to a causal theory is that superluminal signalling is forbidden, which holds in quantum theory. In Bell scenarios, relativistic causality principles like no superluminal signalling are often assumed to follow from the standard no-signalling constraints on correlations. We explore the connections between a range of relativistic principles, including no superluminal signalling and no causal loops, and constraints on correlations that can arise with arbitrary interventions, within multi-party Bell scenarios. This includes standard no-signalling conditions and proposed relaxations allowing phenomena like jamming, where it was suggested that superluminal signalling and causal loops remain impossible. Using our recent framework combining relativistic principles with causal modelling, we show that any theory (classical or non-classical) allowing jamming must rely on causal fine-tuning and superluminal causal influences. Additionally, we show that jamming theories can lead to superluminal sig

Models for quantum state reduction address the quantum measurement problem by suggesting weak modifications to Schrödinger's equation that have no observable effect at microscopic scales, but dominate the dynamics of macroscopic objects. Enforcing linearity of the master equation for such models has long been used as a way of ensuring that modifications to Schrödinger's equation do not introduce a possibility for superluminal signalling. In large classes of quantum state reduction models, however, and in particular in models employing correlated noise, formulating a master equation for the quantum state is prohibitively difficult or impossible. Here, we formulate a witness for superluminal signalling that is applicable to generic quantum state reduction models, including those involving correlated as well as uncorrelated noise. Surprisingly, application of the witness to known models described by linear master equations shows that these may still admit superluminal signalling, unless a particular locality condition is obeyed. In contrast, we show that the witness introduced here provides a necessary and sufficient condition for excluding superluminal signals under all circumstances

We consider optimal signalling and control of discrete-time nonlinear partially observable stochastic systems in state space form. In the first part of the paper, we characterize the operational {\it control-coding capacity}, $C_{FB}$ in bits/second, by an information theoretic optimization problem of encoding signals or messages into randomized controller-encoder strategies, and reproducing the messages at the output of the system using a decoder or estimator with arbitrary small asymptotic error probability. Our analysis of $C_{FB}$ is based on realizations of randomized strategies (controller-encoders), in terms of information states of nonlinear filtering theory, and either uniform or arbitrary distributed random variables (RVs). In the second part of the paper, we analyze the linear-quadratic Gaussian partially observable stochastic system (LQG-POSS). We show that simultaneous signalling and control leads to randomized strategies described by finite-dimensional sufficient statistics, that involve two Kalman-filters, and consist of control, estimation and signalling strategies. We apply decentralized optimization techniques to prove a separation principle, and to derive the opt

Decentralised Autonomous Organisations (DAOs) are a new type of digital organisation that uses blockchain infrastructure (e.g. smart contracts, tokens) to coordinate a group of people around a shared mission. Like all organisations, DAOs must attract sources of funding and other resources, and discover and retain a talented community and workforce. To do this, they must signal their true quality. Yet the characteristics of the environment that DAOs operate in (pseudonymous actors, global scale, permissionless entry and exit) makes this difficult. We apply costly signalling theory to explore the information asymmetry problem in DAOs and some of the strategies (behaviours and investments) and institutional solutions (including better signalling mechanisms) that have evolved to solve this problem.

In this paper we analyze the problem of "apparent" superluminal signalling and retrocausation that can appear for particle detector models when considering non-compactly supported field-detector interactions in quantum field theory in curved spacetimes and in relativistic quantum information protocols. For this purpose, we define a signalling estimator based on an adapted version of the quantum Fisher information to perturbative regimes. This allows us to study how the internal dynamics of the detectors (for example the gap between the detector energy levels) have an impact on the ability of a particle detectors to communicate with one another. Moreover, we show that, very generally, even for detectors with infinite tails in space and time, if the tails decay exponentially, one can define an effective lightcone, outside of which signalling is negligible. This provides concrete evidence supporting the use of non-compact (but exponentially decaying) detector smearings in protocols of relativistic quantum information.

A causal relation between quantum agents, say Alice and Bob, is necessarily mediated by an interaction. Modelling the last one as a reversible quantum channel, an intervention of Alice can have causal influence on Bob's system, modifying correlations between Alice and Bob's systems. Causal influence between quantum systems necessarily allows for signalling. Here we prove a mismatch between causal influence and signalling via direct computation of the two quantities for the Cnot gate. Finally we show a continuity theorem for causal effects of unitary channels: a channel has small causal influence iff it allows for small signalling.

It is a frequent assumption that - via superluminal information transfers - superluminal signals capable of enabling communication are necessarily exchanged in any quantum theory that posits hidden superluminal influences. However, does the presence of hidden superluminal influences automatically imply superluminal signalling and communication? The non-signalling theorem mediates the apparent conflict between quantum mechanics and the theory of special relativity. However, as a 'no-go' theorem there exist two opposing interpretations of the non-signalling constraint: foundational and operational. Concerning Bell's theorem, we argue that Bell employed both interpretations at different times. Bell finally pursued an explicitly operational position on non-signalling which is often associated with ontological quantum theory, e.g., de Broglie-Bohm theory. This position we refer to as "effective non-signalling". By contrast, associated with orthodox quantum mechanics is the foundational position referred to here as "axiomatic non-signalling". In search of a decisive communication-theoretic criterion for differentiating between "axiomatic" and "effective" non-signalling, we employ the ope

Causality is fundamental to science, but it appears in several different forms. One is relativistic causality, which is tied to a space-time structure and forbids signalling outside the future. A second is an operational notion of causation that considers the flow of information between physical systems and interventions on them. In [Vilasini and Colbeck, Phys. Rev. A. 106, 032204 (2022)], we propose a framework for characterising when a causal model can coexist with relativistic principles such as no superluminal signalling, while allowing for cyclic and non-classical causal influences and the possibility of causation without signalling. In a theory without superluminal causation, both superluminal signalling and causal loops are not possible in Minkowski space-time. Here we demonstrate that if we only forbid superluminal signalling, superluminal causation remains possible and show the mathematical possibility of causal loops that can be embedded in a Minkowski space-time without leading to superluminal signalling. The existence of such loops in the given space-time could in principle be operationally verified using interventions. This establishes that the physical principle of no

In this paper, we contribute a multi-faceted study into Pavlovian signalling -- a process by which learned, temporally extended predictions made by one agent inform decision-making by another agent. Signalling is intimately connected to time and timing. In service of generating and receiving signals, humans and other animals are known to represent time, determine time since past events, predict the time until a future stimulus, and both recognize and generate patterns that unfold in time. We investigate how different temporal processes impact coordination and signalling between learning agents by introducing a partially observable decision-making domain we call the Frost Hollow. In this domain, a prediction learning agent and a reinforcement learning agent are coupled into a two-part decision-making system that works to acquire sparse reward while avoiding time-conditional hazards. We evaluate two domain variations: machine agents interacting in a seven-state linear walk, and human-machine interaction in a virtual-reality environment. Our results showcase the speed of learning for Pavlovian signalling, the impact that different temporal representations do (and do not) have on agent

There are two phases of Wnt signalling in early vertebrate embryogenesis: very early, maternal Wnt signalling promotes dorsal development, and slightly later, zygotic Wnt signalling promotes ventral and lateral mesoderm induction. However, recent molecular biology analysis has revealed more complexity among the direct Wnt target genes, with at least five classes. Here in order to test the logic and the dynamics of a new Gene Regulatory Network model suggested by these discoveries we use mathematical modelling based on ordinary differential equations (ODEs). Our mathematical modelling of this Gene Regulatory Network reveals that a simplified model, with one "super-gene" for each class is sufficient to a large extent to describe the regulatory behaviour previously observed experimentally.

In systems biology and pharmacology, large-scale kinetic models are used to study the dynamic response of a system to a specific input or stimulus. While in many applications, a deeper understanding of the input-response behaviour is highly desirable, it is often hindered by the large number of molecular species and the complexity of the interactions. An approach that identifies key molecular species for a given input-response relationship and characterises dynamic properties of states is therefore highly desirable. We introduce the concept of index analysis; it is based on different time- and state-dependent quantities (indices) to identify important dynamic characteristics of molecular species. All indices are defined for a specific pair of input and response variables as well as for a specific magnitude of the input. In application to a large-scale kinetic model of the EGFR signalling cascade, we identified different phases of signal transduction, the peculiar role of Phosphatase3 during signal activation and Ras recycling during signal onset. In addition, we discuss the challenges and pitfalls of interpreting the relevance of molecular species based on knock-out simulation stud

Many biological and social systems show significant levels of collective action. Several cooperation mechanisms have been proposed, yet they have been mostly studied independently. Among these, direct reciprocity supports cooperation on the basis of repeated interactions among individuals. Signals and quorum dynamics may also drive cooperation. Here, we resort to an evolutionary game theoretical model to jointly analyse these two mechanisms and study the conditions in which evolution selects for direct reciprocity, signalling, or their combination. We show that signalling alone leads to higher levels of cooperation than when combined with reciprocity, while offering additional robustness against errors. Specifically, successful strategies in the realm of direct reciprocity are often not selected in the presence of signalling, and memory of past interactions is only exploited opportunistically in case of earlier coordination failure. Differently, signalling always evolves, even when costly. In the light of these results, it may be easier to understand why direct reciprocity has been observed only in a limited number of cases among non-humans, whereas signalling is widespread at all

Plant hormone auxin has critical roles in plant growth, dependent on its heterogeneous distribution in plant tissues. Exactly how auxin transport and developmental processes such as growth coordinate to achieve the precise patterns of auxin observed experimentally is not well understood. Here we use mathematical modelling to examine the interplay between auxin dynamics and growth and their contribution to formation of patterns in auxin distribution in plant tissues. Mathematical models describing the auxin-related signalling pathway, PIN and AUX1 dynamics, auxin transport, and cell growth in plant tissues are derived. A key assumption of our models is the regulation of PIN proteins by the auxin-responsive ARF-Aux/IAA signalling pathway, with upregulation of PIN biosynthesis by ARFs. Models are analysed and solved numerically to examine the long-time behaviour and auxin distribution. Changes in auxin-related signalling processes are shown to be able to trigger transition between passage and spot type patterns in auxin distribution. The model was also shown to be able to generate isolated cells with oscillatory dynamics in levels of components of the auxin signalling pathway which co

We review the characteristics of signalling storms that have been caused by certain common apps and recently observed in cellular networks, leading to system outages. We then develop a mathematical model of a mobile user's signalling behaviour which focuses on the potential of causing such storms, and represent it by a large Markov chain. The analysis of this model allows us to determine the key parameters of mobile user device behaviour that can lead to signalling storms. We then identify the parameter values that will lead to worst case load for the network itself in the presence of such storms. This leads to explicit results regarding the manner in which individual mobile behaviour can cause overload conditions on the network and its signalling servers, and provides insight into how this may be avoided.

Smartphone users and application behaviors add high pressure to apply smart techniques that stabilize the network capacity and consequently improve the end-user experience. The massive increase in smartphone penetration engenders signalling load, which exceeds the network capacity in terms of signaling. The signalling load leads to network congestion, degradation in the network KPIs. The classical way to tackle the signalling is by network expansion. However, this approach is not efficient in terms of capital expenditure (CAPEX) and also in terms of efficient utilization of the network resources. More specifically, the signaling domain becomes overloaded while the data domain are underutilized. In this paper, two UMTS air-interface features; Cell-PCH (paging channel) and enhanced fast dormancy (E-FD) are analyzed to mitigate the signalling load. Practical performance analysis is conducted based on results from commercial UMTS networks. The deployment of these features offers major improvement in network KPIs and significant relief in the signaling load. It is concluded that these two features in addition to several optimization techniques, discussed in this paper, provide solution