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Register a new userA Collaboration Network Model Of Cytokine-Protein Network
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Complex networks provide us a new view for investigation of immune systems. In this paper we collect data through STRING database and present a model with cooperation network theory. The cytokine-protein network model we consider is constituted by two kinds of nodes, one is immune cytokine types which can act as acts, other one is protein type which can act as actors. From act degree distribution that can be well described by typical SPL -shifted power law functions, we find that HRAS.TNFRSF13C.S100A8.S100A1.MAPK8.S100A7.LIF.CCL4.CXCL13 are highly collaborated with other proteins. It reveals that these mediators are important in cytokine-protein network to regulate immune activity. Dyad act degree distribution is another important property to generalized collaboration network. Dyad is two proteins and they appear in one cytokine collaboration relationship. The dyad act degree distribution can be well described by typical SPL functions. The length of the average shortest path is 1.29. These results show that this model could describe the cytokine-protein collaboration preferably
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Recently, the structural controllability theory has been introduced to analyze the Protein-Protein Interaction (PPI) network. The indispensable nodes, which their removal increase the number of driver nodes to control the network, are found essential in PPI network. However, the PPI network is far from complete and there may exist many false-positive or false-negative interactions, which promotes us to question: are these indispensable nodes robust to structural change? Here we systematically investigate the robustness of indispensable nodes of PPI network by removing and adding possible interactions. We found that the indispensable nodes are sensitive to the structural change and very few edges can change the type of many indispensable nodes. The finding may promote our understanding to the control principle of PPI network.
Revealing how a biological network is organized to realize its function is one of the main topics in systems biology. The functional backbone network, defined as the primary structure of the biological network, is of great importance in maintaining the main function of the biological network. We propose a new algorithm, the tinker algorithm, to determine this core structure and apply it in the cell-cycle system. With this algorithm, the backbone network of the cell-cycle network can be determined accurately and efficiently in various models such as the Boolean model, stochastic model, and ordinary differential equation model. Results show that our algorithm is more efficient than that used in the previous research. We hope this method can be put into practical use in relevant future studies.
The network of 5823 cities of Mexico with a population more than 5000 inhabitants is studied. Our analysis is focused to the spectral properties of the adjacency matrix, the small-world properties of the network, the distribution of the clustering coefficients and the degree distribution of the vertices. The connection of these features with the spread of epidemics on this network is also discussed.
Currently, many studies of Alzheimers disease (AD) are investigating the neurobiological factors behind the acquisition of beta-amyloid (A), pathologic tau (T), and neurodegeneration ([N]) biomarkers from neuroimages. However, a system-level mechanism of how these neuropathological burdens promote neurodegeneration and why AD exhibits characteristic progression is largely elusive. In this study, we combined the power of systems biology and network neuroscience to understand the dynamic interaction and diffusion process of AT[N] biomarkers from an unprecedented amount of longitudinal Amyloid PET scan, MRI imaging, and DTI data. Specifically, we developed a network-guided biochemical model to jointly (1) model the interaction of AT[N] biomarkers at each brain region and (2) characterize their propagation pattern across the fiber pathways in the structural brain network, where the brain resilience is also considered as a moderator of cognitive decline. Our biochemical model offers a greater mathematical insight to understand the physiopathological mechanism of AD progression by studying the system dynamics and stability. Thus, an in-depth system-level analysis allows us to gain a new understanding of how AT[N] biomarkers spread throughout the brain, capture the early sign of cognitive decline, and predict the AD progression from the preclinical stage.
Complexes of physically interacting proteins are one of the fundamental functional units responsible for driving key biological mechanisms within the cell. Their identification is therefore necessary not only to understand complex formation but also the higher level organization of the cell. With the advent of high-throughput techniques in molecular biology, significant amount of physical interaction data has been cataloged from organisms such as yeast, which has in turn fueled computational approaches to systematically mine complexes from the network of physical interactions among proteins (PPI network). In this survey, we review, classify and evaluate some of the key computational methods developed till date for the identification of protein complexes from PPI networks. We present two insightful taxonomies that reflect how these methods have evolved over the years towards improving automated complex prediction. We also discuss some open challenges facing accurate reconstruction of complexes, the crucial ones being presence of high proportion of errors and noise in current high-throughput datasets and some key aspects overlooked by current complex detection methods. We hope this review will not only help to condense the history of computational complex detection for easy reference, but also provide valuable insights to drive further research in this area.
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