Collaborative Inference of Coexisting Information Diffusions

Recently, \textit{diffusion history inference} has become an emerging research topic due to its great benefits for various applications, whose purpose is to reconstruct the missing histories of information diffusion traces according to incomplete observations. The existing methods, however, often focus only on single information diffusion trace, while in a real-world social network, there often coexist multiple information diffusions over the same network. In this paper, we propose a novel approach called Collaborative Inference Model (CIM) for the problem of the inference of coexisting information diffusions. By exploiting the synergism between the coexisting information diffusions, CIM holistically models multiple information diffusions as a sparse 4th-order tensor called Coexisting Diffusions Tensor (CDT) without any prior assumption of diffusion models, and collaboratively infers the histories of the coexisting information diffusions via a low-rank approximation of CDT with a fusion of heterogeneous constraints generated from additional data sources. To improve the efficiency, we further propose an optimal algorithm called Time Window based Parallel Decomposition Algorithm (TWPDA), which can speed up the inference without compromise on the accuracy by utilizing the temporal locality of information diffusions. The extensive experiments conducted on real world datasets and synthetic datasets verify the effectiveness and efficiency of CIM and TWPDA

Data based identification and prediction of nonlinear and complex dynamical systems

We thank Dr. R. Yang (formerly at ASU), Dr. R.-Q. Su (formerly at ASU), and Mr. Zhesi Shen for their contributions to a number of original papers on which this Review is partly based. This work was supported by ARO under Grant No. W911NF-14-1-0504. W.-X. Wang was also supported by NSFC under Grants No. 61573064 and No. 61074116, as well as by the Fundamental Research Funds for the Central Universities, Beijing Nova Programme.Peer reviewedPostprin

Joint Inference of Structure and Diffusion in Partially Observed Social Networks

Access to complete data in large scale networks is often infeasible. Therefore, the problem of missing data is a crucial and unavoidable issue in analysis and modeling of real-world social networks. However, most of the research on different aspects of social networks do not consider this limitation. One effective way to solve this problem is to recover the missing data as a pre-processing step. The present paper tries to infer the unobserved data from both diffusion network and network structure by learning a model from the partially observed data. We develop a probabilistic generative model called "DiffStru" to jointly discover the hidden links of network structure and the omitted diffusion activities. The interrelations among links of nodes and cascade processes are utilized in the proposed method via learning coupled low dimensional latent factors. In addition to inferring the unseen data, the learned latent factors may also help network classification problems such as community detection. Simulation results on synthetic and real-world datasets show the excellent performance of the proposed method in terms of link prediction and discovering the identity and infection time of invisible social behaviors

Network deconvolution as a general method to distinguish direct dependencies in networks

Recognizing direct relationships between variables connected in a network is a pervasive problem in biological, social and information sciences as correlation-based networks contain numerous indirect relationships. Here we present a general method for inferring direct effects from an observed correlation matrix containing both direct and indirect effects. We formulate the problem as the inverse of network convolution, and introduce an algorithm that removes the combined effect of all indirect paths of arbitrary length in a closed-form solution by exploiting eigen-decomposition and infinite-series sums. We demonstrate the effectiveness of our approach in several network applications: distinguishing direct targets in gene expression regulatory networks; recognizing directly interacting amino-acid residues for protein structure prediction from sequence alignments; and distinguishing strong collaborations in co-authorship social networks using connectivity information alone. In addition to its theoretical impact as a foundational graph theoretic tool, our results suggest network deconvolution is widely applicable for computing direct dependencies in network science across diverse disciplines.National Institutes of Health (U.S.) (grant R01 HG004037)National Institutes of Health (U.S.) (grant HG005639)Swiss National Science Foundation (Fellowship)National Science Foundation (U.S.) (NSF CAREER Award 0644282

A Study Of Computational Problems In Computational Biology And Social Networks: Cancer Informatics And Cascade Modelling

It is undoubtedly that everything in this world is related and nothing independently exists. Entities interact together to form groups, resulting in many complex networks. Examples involve functional regulation models of proteins in biology, communities of people within social network. Since complex networks are ubiquitous in daily life, network learning had been gaining momentum in a variety of discipline like computer science, economics and biology. This call for new technique in exploring the structure as well as the interactions of network since it provides insight in understanding how the network works and deepening our knowledge of the subject in hand. For example, uncovering proteins modules helps us understand what causes lead to certain disease and how protein co-regulate each others. Therefore, my dissertation takes on problems in computational biology and social network: cancer informatics and cascade model-ling. In cancer informatics, identifying specific genes that cause cancer (driver genes) is crucial in cancer research. The more drivers identified, the more options to treat the cancer with a drug to act on that gene. However, identifying driver gene is not easy. Cancer cells are undergoing rapid mutation and are compromised in regards to the body\u27s normally DNA repair mechanisms. I employed Markov chain, Bayesian network and graphical model to identify cancer drivers. I utilize heterogeneous sources of information to discover cancer drivers and unlocking the mechanism behind cancer. Above all, I encode various pieces of biological information to form a multi-graph and trigger various Markov chains in it and rank the genes in the aftermath. We also leverage probabilistic mixed graphical model to learn the complex and uncertain relationships among various bio-medical data. On the other hand, diffusion of information over the network had drawn up great interest in research community. For example, epidemiologists observe that a person becomes ill but they can neither determine who infected the patient nor the infection rate of each individual. Therefore, it is critical to decipher the mechanism underlying the process since it validates efforts for preventing from virus infections. We come up with a new modeling to model cascade data in three different scenario