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Optimizing the performance of multimodal freight transport networks involves adequately balancing the interplay between costs, volumes, times of departure and arrival, and times of travel. In order to study this interplay, we propose an assignment model that is able to efficiently determine flows and costs in a multimodal network. The model is based on a so-called user equilibrium principle, which is at the basis of Dynamic Traffic Assignment problems. This principle takes into account transport demands to be shipped using vehicles that transport single freight units (such as trucks) or multiple freight units (such as trains and barges, where demand should be bundled to reach efficient operations). Given a particular demand, the proposed model provides an assignment of the demand over the available modes of transport. The outcome of the model, i.e., the equilibrium point, minimizes users’ generalized costs, expressed as a function of mode, travel time and related congestion, and waiting time for bundling sufficient demand in order to fill a vehicle. The model deals with these issues across a doubly-dynamic time scale and in an integrated manner. One dynamic involves a learning dynamic converging towards an equilibrium (day-to-day) situation, reflecting the reaction of the players towards the action of the others. Another dynamic considers the possible departure time that results in minimum expected costs, also due to the fact that players mutually influence each other on the choice of departure times, due to congestion effects and costs for early/late arrival of freight units. This is a choice within a given time horizon such as a day or a week. We present a study on the influence and sensitivity of different model parameters, in order to analyse the implications on strategic decisions, fostering a target modal share for freight transportation. We also study under which conditions the different modes can be substitutes for each other.  相似文献   
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Traditionally, the diffusion of acetylcholine (ACh) from a neuron to cardiac muscle in a neuroeffector junction has been modeled as radial diffusion from a nerve ending into a spherical homogeneous medium. Various microscopic structures in the heart may or may not influence the spatial distribution of ACh within neuroeffector junctions. To determine the effect of microscopic anatomy on the diffusion of ACh in neuroeffector junctions, we simulated the diffusion of ACh in a two-dimensional inhomogeneous geometry that was based on micrographs of neuroeffector junctions in the sinus node. ACh was released at sites adjacent to a neuron. Simulations showed that the times of peak concentration after release and the peak concentrations per se were distributed symmetrically above and below and to the right and left of the neuron, but not radially about the neuron. We conclude that the diffusion of ACh in the neuroeffector junctions of the sinus node cannot be predicted well by a mathematical model that assumes radial diffusion in a spherical and homogeneous medium.  相似文献   
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Using immunocytochemical methods, a severe loss of substance P, but not of enkephalin, cholecystokinin and serotonin containing fibers was observed in lamina IX of the spinal cords from 4 amyotrophic lateral sclerosis cases. Substance P-fibers were decreased before degeneration of motoneurons. They were normal in the remaining spinal gray matter.  相似文献   
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Human adenovirus cloning vectors based on infectious bacterial plasmids   总被引:8,自引:0,他引:8  
By making use of the fact that human adenovirus DNA circularizes in infected cells, and that circular forms of the viral genome are infectious, we have developed an improved adenovirus-based cloning system. A deletion mutant of adenovirus type 5 (Ad5) with deletions in early regions 1 (E1) and 3 (E3) was converted to a bacterial plasmid which can regenerate infectious virus following transfection into human 293 cells. A single XbaI recognition site in the deleted E3 region serves as a site for the insertion of foreign DNA. We have used this system to clone a number of genes into the Ad5 genome and describe the insertion of the neomycin/G418 resistance marker into Ad5 as an example.  相似文献   
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