K.-I. Goh

A network of disorders and disease genes linked by known disorder-gene associations offers a platform to explore in a single graph-theoretic framework all known phenotype and disease gene associations, indicating the common genetic origin of many diseases. Genes associated with similar disorders show both higher likelihood of physical interactions between their products and higher expression profiling similarity for their transcripts, supporting the existence of distinct disease-specific functional modules. We find that essential human genes are likely to encode hub proteins and are expressed widely in most tissues. This suggests that disease genes also would play a central role in the human interactome. In contrast, we find that the vast majority of disease genes are nonessential and show no tendency to encode hub proteins, and their expression pattern indicates that they are localized in the functional periphery of the network. A selection-based model explains the observed difference between essential and disease genes and also suggests that diseases caused by somatic mutations should not be peripheral, a prediction we confirm for cancer genes.

We study a problem of data packet transport in scale-free networks whose degree distribution follows a power law with the exponent gamma. Load, or "betweenness centrality," of a vertex is the accumulated total number of data packets passing through that vertex when every pair of vertices sends and receives a data packet along the shortest path connecting the pair. It is found that the load distribution follows a power law with the exponent delta approximately 2.2(1), insensitive to different values of gamma in the range, 2 < gamma < or = 3, and different mean degrees, which is valid for both undirected and directed cases. Thus, we conjecture that the load exponent is a universal quantity to characterize scale-free networks.

The dynamics of many social, technological and economic phenomena are driven by individual human actions, turning the quantitative understanding of human behavior into a central question of modern science. Current models of human dynamics, used from risk assessment to communications, assume that human actions are randomly distributed in time and thus well approximated by Poisson processes. Here we provide direct evidence that for five human activity patterns, such as email and letter based communications, web browsing, library visits and stock trading, the timing of individual human actions follow non-Poisson statistics, characterized by bursts of rapidly occurring events separated by long periods of inactivity. We show that the bursty nature of human behavior is a consequence of a decision based queuing process: when individuals execute tasks based on some perceived priority, the timing of the tasks will be heavy tailed, most tasks being rapidly executed, while a few experiencing very long waiting times. In contrast, priority blind execution is well approximated by uniform interevent statistics. We discuss two queuing models that capture human activity. The first model assumes that there are no limitations on the number of tasks an individual can handle at any time, predicting that the waiting time of the individual tasks follow a heavy tailed distribution P(tau(w)) approximately tau(w)(-alpha) with alpha=3/2. The second model imposes limitations on the queue length, resulting in a heavy tailed waiting time distribution characterized by alpha=1. We provide empirical evidence supporting the relevance of these two models to human activity patterns, showing that while emails, web browsing and library visitation display alpha=1, the surface mail based communication belongs to the alpha=3/2 universality class. Finally, we discuss possible extension of the proposed queuing models and outline some future challenges in exploring the statistical mechanics of human dynamics.

The dynamics of a wide range of real systems, from email patterns to earthquakes, display a bursty, intermittent nature, characterized by short timeframes of intensive activity followed by long times of no or reduced activity. The understanding of the origin of such bursty patterns is hindered by the lack of tools to compare different systems using a common framework. We introduce two measures to distinguish the mechanisms responsible for the bursty nature of real signals, changes in the interevent times and memory. We find that while the burstiness of natural phenomena is rooted in both the interevent time distribution and memory, for human dynamics memory is weak, and the bursty character is due to changes in the interevent time distribution. Finally, we show that current models lack in their ability to reproduce the activity pattern observed in real systems, opening up new avenues for future work.