Given a social network G and a positive integer k, the influence maximization problem asks for k nodes (in G) whose adoptions of a certain idea or product can trigger the largest expected number of follow-up adoptions by the remaining nodes. This problem has been extensively studied in the literature, and the state-of-the-art technique runs in O((k + ℓ)(n + m) log n/ε 2 ) expected time and returns a (1 − 1/e − ε)-approximate solution with at least 1 − 1/n ℓ probability.This paper presents an influence maximization algorithm that provides the same worst-case guarantees as the state of the art, but offers significantly improved empirical efficiency. The core of our algorithm is a set of estimation techniques based on martingales, a classic statistical tool. Those techniques not only provide accurate results with small computation overheads, but also enable our algorithm to support a larger class of information diffusion models than existing methods do. We experimentally evaluate our algorithm against the states of the art under several popular diffusion models, using real social networks with up to 1.4 billion edges. Our experimental results show that the proposed algorithm consistently outperforms the states of the art in terms of computation efficiency, and is often orders of magnitude faster.
BackgroundZero-dimensional (lumped parameter) and one dimensional models, based on simplified representations of the components of the cardiovascular system, can contribute strongly to our understanding of circulatory physiology. Zero-D models provide a concise way to evaluate the haemodynamic interactions among the cardiovascular organs, whilst one-D (distributed parameter) models add the facility to represent efficiently the effects of pulse wave transmission in the arterial network at greatly reduced computational expense compared to higher dimensional computational fluid dynamics studies. There is extensive literature on both types of models.Method and ResultsThe purpose of this review article is to summarise published 0D and 1D models of the cardiovascular system, to explore their limitations and range of application, and to provide an indication of the physiological phenomena that can be included in these representations. The review on 0D models collects together in one place a description of the range of models that have been used to describe the various characteristics of cardiovascular response, together with the factors that influence it. Such models generally feature the major components of the system, such as the heart, the heart valves and the vasculature. The models are categorised in terms of the features of the system that they are able to represent, their complexity and range of application: representations of effects including pressure-dependent vessel properties, interaction between the heart chambers, neuro-regulation and auto-regulation are explored. The examination on 1D models covers various methods for the assembly, discretisation and solution of the governing equations, in conjunction with a report of the definition and treatment of boundary conditions. Increasingly, 0D and 1D models are used in multi-scale models, in which their primary role is to provide boundary conditions for sophisticate, and often patient-specific, 2D and 3D models, and this application is also addressed. As an example of 0D cardiovascular modelling, a small selection of simple models have been represented in the CellML mark-up language and uploaded to the CellML model repository http://models.cellml.org/. They are freely available to the research and education communities.ConclusionEach published cardiovascular model has merit for particular applications. This review categorises 0D and 1D models, highlights their advantages and disadvantages, and thus provides guidance on the selection of models to assist various cardiovascular modelling studies. It also identifies directions for further development, as well as current challenges in the wider use of these models including service to represent boundary conditions for local 3D models and translation to clinical application.
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