96 research outputs found
Black swans or dragon kings? A simple test for deviations from the power law
We develop a simple test for deviations from power law tails, which is based
on the asymptotic properties of the empirical distribution function. We use
this test to answer the question whether great natural disasters, financial
crashes or electricity price spikes should be classified as dragon kings or
'only' as black swans
Dragon-kings: mechanisms, statistical methods and empirical evidence
This introductory article presents the special Discussion and Debate volume
"From black swans to dragon-kings, is there life beyond power laws?" published
in Eur. Phys. J. Special Topics in May 2012. We summarize and put in
perspective the contributions into three main themes: (i) mechanisms for
dragon-kings, (ii) detection of dragon-kings and statistical tests and (iii)
empirical evidence in a large variety of natural and social systems. Overall,
we are pleased to witness significant advances both in the introduction and
clarification of underlying mechanisms and in the development of novel
efficient tests that demonstrate clear evidence for the presence of
dragon-kings in many systems. However, this positive view should be balanced by
the fact that this remains a very delicate and difficult field, if only due to
the scarcity of data as well as the extraordinary important implications with
respect to hazard assessment, risk control and predictability.Comment: 20 page
Longevity‐related molecular pathways are subject to midlife “switch” in humans
Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that opposed, the signature. We profiled Rapamycin in nondividing primary human myotubes (n = 32 HTA 2.0 arrays) and determined the transcript signature for reactive oxygen species in neurons, confirming that our age signature was largely regulated in the “pro‐longevity” direction. Quantitative network modeling demonstrated that age‐regulated ncRNA equaled the contribution of protein‐coding RNA within structures, but tended to have a lower heritability, implying lncRNA may better reflect environmental influences. Genes ECSIT, UNC13, and SKAP2 contributed to a network that did not respond to Rapamycin, and was associated with “neuron apoptotic processes” in protein–protein interaction analysis (FDR = 2.4%). ECSIT links inflammation with the continued age‐related downwards trajectory of mitochondrial complex I gene expression (FDR < 0.01%), implying that sustained inhibition of ECSIT may be maladaptive. The present observations link, for the first time, model organism longevity programs with the endogenous but temporary genome‐wide responses to aging in humans, revealing a pattern that may ultimately underpin personalized rates of health span.peerReviewe
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