4,735 research outputs found

    A meaningful expansion around detailed balance

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    We consider Markovian dynamics modeling open mesoscopic systems which are driven away from detailed balance by a nonconservative force. A systematic expansion is obtained of the stationary distribution around an equilibrium reference, in orders of the nonequilibrium forcing. The first order around equilibrium has been known since the work of McLennan (1959), and involves the transient irreversible entropy flux. The expansion generalizes the McLennan formula to higher orders, complementing the entropy flux with the dynamical activity. The latter is more kinetic than thermodynamic and is a possible realization of Landauer's insight (1975) that, for nonequilibrium, the relative occupation of states also depends on the noise along possible escape routes. In that way nonlinear response around equilibrium can be meaningfully discussed in terms of two main quantities only, the entropy flux and the dynamical activity. The expansion makes mathematical sense as shown in the simplest cases from exponential ergodicity.Comment: 19 page

    Dynamical fluctuations for semi-Markov processes

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    We develop an Onsager-Machlup-type theory for nonequilibrium semi-Markov processes. Our main result is an exact large time asymptotics for the joint probability of the occupation times and the currents in the system, establishing some generic large deviation structures. We discuss in detail how the nonequilibrium driving and the non-exponential waiting time distribution influence the occupation-current statistics. The violation of the Markov condition is reflected in the emergence of a new type of nonlocality in the fluctuations. Explicit solutions are obtained for some examples of driven random walks on the ring.Comment: Minor changes, accepted for publication in Journal of Physics

    Non-equilibrium stationary state of a two-temperature spin chain

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    A kinetic one-dimensional Ising model is coupled to two heat baths, such that spins at even (odd) lattice sites experience a temperature TeT_{e} (% T_{o}). Spin flips occur with Glauber-type rates generalised to the case of two temperatures. Driven by the temperature differential, the spin chain settles into a non-equilibrium steady state which corresponds to the stationary solution of a master equation. We construct a perturbation expansion of this master equation in terms of the temperature difference and compute explicitly the first two corrections to the equilibrium Boltzmann distribution. The key result is the emergence of additional spin operators in the steady state, increasing in spatial range and order of spin products. We comment on the violation of detailed balance and entropy production in the steady state.Comment: 11 pages, 1 figure, Revte

    Sarcopenia predicts 5-year mortality in older adults with intellectual disabilities

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    Background: People with intellectual disabilities (ID) have a lower life expectancy than their peers without ID. A contributing factor to the lower life expectancy and early mortality could be sarcopenia: low muscle mass and low muscle function. In the general population, sarcopenia strongly predicts early mortality, but this association is unknown in people with ID. Therefore, this study aims to explore the association between sarcopenia and 5-year mortality in older adults with ID. Methods: In the Healthy Ageing and Intellectual Disabilities (HA-ID) study, the prevalence of sarcopenia was measured at baseline among 884 older adults (≥50 years) with ID. All-cause mortality was measured over a 5-year follow-up period. Univariable and multivariable Cox proportional hazard models were applied to determine the association between sarcopenia (no sarcopenia, pre-sarcopenia, sarcopenia, severe sarcopenia) and early mortality, adjusted for age, sex, level of ID, presence of Down syndrome, and co-morbidity (chronic obstructive pulmonary disease, diabetes type 2 and metabolic syndrome). Results: The unadjusted hazard ratio (HR) for sarcopenia was 2.28 [95% confidence interval (CI) 1.48–3.42], P &lt; 0.001), and 2.40 (95% CI 1.40–4.10, P = 0.001) for severe sarcopenia. When adjusted for age, sex, level of ID, and Down syndrome, sarcopenia (HR = 1.72, 95% CI 1.08–2.75, P = 0.022) and severe sarcopenia (HR = 1.86, 95% CI 1.07–3.23, P = 0.028) were significantly associated with early mortality. When additionally adjusted for co-morbidity, the adjusted HR decreased to 1.62 (95% CI 1.02–2.59, P = 0.043) and 1.81 (95% CI 1.04–3.15, P = 0.035) for sarcopenia and severe sarcopenia, respectively. Conclusion: Sarcopenia is an independent risk factor for early mortality in older adults with ID over a 5-year follow-up period. Our results stress the need to delay the incidence and development of sarcopenia in older adults with ID.</p

    The Measure-theoretic Identity Underlying Transient Fluctuation Theorems

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    We prove a measure-theoretic identity that underlies all transient fluctuation theorems (TFTs) for entropy production and dissipated work in inhomogeneous deterministic and stochastic processes, including those of Evans and Searles, Crooks, and Seifert. The identity is used to deduce a tautological physical interpretation of TFTs in terms of the arrow of time, and its generality reveals that the self-inverse nature of the various trajectory and process transformations historically relied upon to prove TFTs, while necessary for these theorems from a physical standpoint, is not necessary from a mathematical one. The moment generating functions of thermodynamic variables appearing in the identity are shown to converge in general only in a vertical strip in the complex plane, with the consequence that a TFT that holds over arbitrary timescales may fail to give rise to an asymptotic fluctuation theorem for any possible speed of the corresponding large deviation principle. The case of strongly biased birth-death chains is presented to illustrate this phenomenon. We also discuss insights obtained from our measure-theoretic formalism into the results of Saha et. al. on the breakdown of TFTs for driven Brownian particles

    Is there an integrative center in the vertebrate brain-stem? A robotic evaluation of a model of the reticular formation viewed as an action selection device

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    Neurobehavioral data from intact, decerebrate, and neonatal rats, suggests that the reticular formation provides a brainstem substrate for action selection in the vertebrate central nervous system. In this article, Kilmer, McCulloch and Blum’s (1969, 1997) landmark reticular formation model is described and re-evaluated, both in simulation and, for the first time, as a mobile robot controller. Particular model configurations are found to provide effective action selection mechanisms in a robot survival task using either simulated or physical robots. The model’s competence is dependent on the organization of afferents from model sensory systems, and a genetic algorithm search identified a class of afferent configurations which have long survival times. The results support our proposal that the reticular formation evolved to provide effective arbitration between innate behaviors and, with the forebrain basal ganglia, may constitute the integrative, ’centrencephalic’ core of vertebrate brain architecture. Additionally, the results demonstrate that the Kilmer et al. model provides an alternative form of robot controller to those usually considered in the adaptive behavior literature

    Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

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    It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

    Levy targeting and the principle of detailed balance

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    We investigate confined L\'{e}vy flights under premises of the principle of detailed balance. The master equation admits a transformation to L\'{e}vy - Schr\"{o}dinger semigroup dynamics (akin to a mapping of the Fokker-Planck equation into the generalized diffusion equation). We solve a stochastic targeting problem for arbitrary stability index 0<ÎĽ<20<\mu <2 of L\'{e}vy drivers: given an invariant probability density function (pdf), specify the jump - type dynamics for which this pdf is a long-time asymptotic target. Our ("ÎĽ\mu-targeting") method is exemplified by Cauchy family and Gaussian target pdfs. We solve the reverse engineering problem for so-called L\'{e}vy oscillators: given a quadratic semigroup potential, find an asymptotic pdf for the associated master equation for arbitrary ÎĽ\mu

    Time dependence of breakdown in a global fiber-bundle model with continuous damage

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    A time-dependent global fiber-bundle model of fracture with continuous damage is formulated in terms of a set of coupled non-linear differential equations. A first integral of this set is analytically obtained. The time evolution of the system is studied by applying a discrete probabilistic method. Several results are discussed emphasizing their differences with the standard time-dependent model. The results obtained show that with this simple model a variety of experimental observations can be qualitatively reproduced.Comment: APS style, two columns, 4 figures. To appear in Phys. Rev.
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