862 resultados para EVOLUTIONARY


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To understand the evolution of bipedalism among the homnoids in an ecological context we need to be able to estimate theenerrgetic cost of locomotion in fossil forms. Ideally such an estimate would be based entirely on morphology since, except for the rare instances where footprints are preserved, this is hte only primary source of evidence available. In this paper we use evolutionary robotics techniques (genetic algoritms, pattern generators and mechanical modeling) to produce a biomimentic simulation of bipedalism based on human body dimensions. The mechnaical simulation is a seven-segment, two-dimensional model with motive force provided by tension generators representing the major muscle groups acting around the lower-limb joints. Metabolic energy costs are calculated from the muscel model, and bipedal gait is generated using a finite-state pattern generator whose parameters are produced using a genetic algorithm with locomotor economy (maximum distance for a fixed energy cost) as the fitness criterion. The model is validated by comparing the values it generates with those for modern humans. The result (maximum efficiency of 200 J m-1) is within 15% of the experimentally derived value, which is very encouraging and suggests that this is a useful analytic technique for investigating the locomotor behaviour of fossil forms. Initial work suggests that in the future this technique could be used to estimate other locomotor parameters such as top speed. In addition, the animations produced by this technique are qualitatively very convincing, which suggests that this may also be a useful technique for visualizing bipedal locomotion.

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This paper combines the idea of a hierarchical distributed genetic algorithm with different inter-agent partnering strategies. Cascading clusters of sub-populations are built from bottom up, with higher-level sub-populations optimising larger parts of the problem. Hence higher-level sub-populations search a larger search space with a lower resolution whilst lower-level sub-populations search a smaller search space with a higher resolution. The effects of different partner selection schemes amongst the agents on solution quality are examined for two multiple-choice optimisation problems. It is shown that partnering strategies that exploit problem-specific knowledge are superior and can counter inappropriate (sub-) fitness measurements.

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This paper combines the idea of a hierarchical distributed genetic algorithm with different inter-agent partnering strategies. Cascading clusters of sub-populations are built from bottom up, with higher-level sub-populations optimising larger parts of the problem. Hence higher-level sub-populations search a larger search space with a lower resolution whilst lower-level sub-populations search a smaller search space with a higher resolution. The effects of different partner selection schemes for (sub-)fitness evaluation purposes are examined for two multiple-choice optimisation problems. It is shown that random partnering strategies perform best by providing better sampling and more diversity.

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This paper combines the idea of a hierarchical distributed genetic algorithm with different inter-agent partnering strategies. Cascading clusters of sub-populations are built from bottom up, with higher-level sub-populations optimising larger parts of the problem. Hence higher-level sub-populations search a larger search space with a lower resolution whilst lower-level sub-populations search a smaller search space with a higher resolution. The effects of different partner selection schemes amongst the agents on solution quality are examined for two multiple-choice optimisation problems. It is shown that partnering strategies that exploit problem-specific knowledge are superior and can counter inappropriate (sub-) fitness measurements.

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Evolutionary algorithms alone cannot solve optimization problems very efficiently since there are many random (not very rational) decisions in these algorithms. Combination of evolutionary algorithms and other techniques have been proven to be an efficient optimization methodology. In this talk, I will explain the basic ideas of our three algorithms along this line (1): Orthogonal genetic algorithm which treats crossover/mutation as an experimental design problem, (2) Multiobjective evolutionary algorithm based on decomposition (MOEA/D) which uses decomposition techniques from traditional mathematical programming in multiobjective optimization evolutionary algorithm, and (3) Regular model based multiobjective estimation of distribution algorithms (RM-MEDA) which uses the regular property and machine learning methods for improving multiobjective evolutionary algorithms.

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International audience

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In Part 1 of this thesis, we propose that biochemical cooperativity is a fundamentally non-ideal process. We show quantal effects underlying biochemical cooperativity and highlight apparent ergodic breaking at small volumes. The apparent ergodic breaking manifests itself in a divergence of deterministic and stochastic models. We further predict that this divergence of deterministic and stochastic results is a failure of the deterministic methods rather than an issue of stochastic simulations.

Ergodic breaking at small volumes may allow these molecular complexes to function as switches to a greater degree than has previously been shown. We propose that this ergodic breaking is a phenomenon that the synapse might exploit to differentiate Ca$^{2+}$ signaling that would lead to either the strengthening or weakening of a synapse. Techniques such as lattice-based statistics and rule-based modeling are tools that allow us to directly confront this non-ideality. A natural next step to understanding the chemical physics that underlies these processes is to consider \textit{in silico} specifically atomistic simulation methods that might augment our modeling efforts.

In the second part of this thesis, we use evolutionary algorithms to optimize \textit{in silico} methods that might be used to describe biochemical processes at the subcellular and molecular levels. While we have applied evolutionary algorithms to several methods, this thesis will focus on the optimization of charge equilibration methods. Accurate charges are essential to understanding the electrostatic interactions that are involved in ligand binding, as frequently discussed in the first part of this thesis.

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The quest for robust heuristics that are able to solve more than one problem is ongoing. In this paper, we present, discuss and analyse a technique called Evolutionary Squeaky Wheel Optimisation and apply it to two different personnel scheduling problems. Evolutionary Squeaky Wheel Optimisation improves the original Squeaky Wheel Optimisation’s effectiveness and execution speed by incorporating two additional steps (Selection and Mutation) for added evolution. In the Evolutionary Squeaky Wheel Optimisation, a cycle of Analysis-Selection-Mutation-Prioritization-Construction continues until stopping conditions are reached. The aim of the Analysis step is to identify below average solution components by calculating a fitness value for all components. The Selection step then chooses amongst these underperformers and discards some probabilistically based on fitness. The Mutation step further discards a few components at random. Solutions can become incomplete and thus repairs may be required. The repair is carried out by using the Prioritization step to first produce priorities that determine an order by which the following Construction step then schedules the remaining components. Therefore, improvements in the Evolutionary Squeaky Wheel Optimisation is achieved by selective solution disruption mixed with iterative improvement and constructive repair. Strong experimental results are reported on two different domains of personnel scheduling: bus and rail driver scheduling and hospital nurse scheduling.

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The pan-Myosin Heavy Chain (pan-MyHC) marker MF20 have been reported to show similar, homogeneous signal in the myocardial segments of the heart of teleosts and tetrapods. However, in an ongoing study of the myocardial structure of the dogfish (Scyliorhinus canicula; Chondrichthyes), we observed differential immunostaining of the cardiac segments using another pan-MyHC, the A4.1025 antibody. In order to investigate the relevance of this finding for better understanding of the morphology and evolution of the vertebrate heart, we performed immunohistochemistry, slot blot and western blot in several species of chondrichthyans, actinopterygians and mammals using the above mentioned antibodies. In the dogfish heart, A4.1025 and MF20 specifically recognized MyHC isoforms, although with different degree of affinity. MF20 reactivity was homogeneous and high in all the myocardial segments. However, A4.1025 reactivity was heterogeneous. It was high in the sinus venosus (external layer), atrium and atrioventricular region, low in the ventricle and conus arteriosus, and null in the internal layer of the sinus venosus. A heterogeneous pattern of A4.1025 immunoreactivity was also detected in two other elasmobranchs, a holocephalan, a polypteryform and an acipenseriform. In all of these species, MF20 immunoreactivity was homogeneous. In addition, both markers showed a homogeneous immunoreactivity pattern in teleosts and mammals. Our results indicate that in the hearts of ancient gnathostomes, in all of which a conspicuous conus arteriosus exists, one or more MyHC isoforms with low affinity for A4.1025 show segment-specific distributions. Thus, A4.1025 appears to be an appropriated marker to identify the cardiac segments and their boundaries. We propose that the segmentspecific distribution of MyHC isoforms may generate a particular type of myocardial contractility associated with the presence of a conus arteriosus.

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The evolution of CRISPR–cas loci, which encode adaptive immune systems in archaea and bacteria, involves rapid changes, in particular numerous rearrangements of the locus architecture and horizontal transfer of complete loci or individual modules. These dynamics complicate straightforward phylogenetic classification, but here we present an approach combining the analysis of signature protein families and features of the architecture of cas loci that unambiguously partitions most CRISPR–cas loci into distinct classes, types and subtypes. The new classification retains the overall structure of the previous version but is expanded to now encompass two classes, five types and 16 subtypes. The relative stability of the classification suggests that the most prevalent variants of CRISPR–Cas systems are already known. However, the existence of rare, currently unclassifiable variants implies that additional types and subtypes remain to be characterized.