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H. Eugene Stanley

Researcher at Boston University

Publications -  1208
Citations -  134813

H. Eugene Stanley is an academic researcher from Boston University. The author has contributed to research in topics: Complex network & Phase transition. The author has an hindex of 154, co-authored 1190 publications receiving 122321 citations. Previous affiliations of H. Eugene Stanley include University of North Carolina at Chapel Hill & Wesleyan University.

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Suppressing disease spreading by using information diffusion on multiplex networks.

TL;DR: In this article, the authors investigated the coevolution mechanisms and dynamics between information and disease spreading by utilizing real data and a proposed spreading model on multiplex network and found that there is an optimal information transmission rate that markedly suppresses the disease spreading.
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Identifying the protein folding nucleus using molecular dynamics.

TL;DR: A nucleation scenario, in which a few well-defined contacts are formed with high probability in the transition state ensemble of conformations, and Amino acid residues participating in those contacts may serve as "accelerator pedals" used by molecular evolution to control protein folding rate.
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Scale-Independent Measures and Pathologic Cardiac Dynamics

TL;DR: It is found that scale-independent measures effectively distinguish healthy from pathologic behavior and a new two-variable scale- independent measure that could be clinically useful is proposed.
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Quantifying and modeling long-range cross correlations in multiple time series with applications to world stock indices

TL;DR: A significant fraction of the world index cross correlations can be explained by the global factor, which supports the utility of the GFM and is demonstrated in applications in forecasting risks at the world level, and in finding uncorrelated individual indices.
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Endogenous circadian rhythm in an index of cardiac vulnerability independent of changes in behavior

TL;DR: The sharp peak in the scaling exponent at the circadian phase coinciding with the period of highest cardiac vulnerability observed in epidemiological studies suggests that endogenous circadian-mediated influences on cardiac control may be involved in the day/night pattern of adverse cardiac events in vulnerable individuals.