Positive Feedback, Memory and the Predictability of Earthquakes

We review the "critical point" concept for large earthquakes and enlarge it in the framework of so-called "finite-time singularities". The singular behavior associated with accelerated seismic release is shown to result from a positive feedback of the seismic activity on its release rate. The most important mechanisms for such positive feedback are presented. We introduce and solve analytically a novel simple model of geometrical positive feedback in which the stress shadow cast by the last large earthquake is progressively fragmented by the increasing tectonic stress. Finally, we present a somewhat speculative figure that tends to support a mechanism based on the decay of stress shadows. This figure suggests that a large earthquake in Southern California of size similar to the 1812 great event is maturing.Comment: PostScript document of 18 pages + 2 eps figure

Oscillatory Finite-Time Singularities in Finance, Population and Rupture

We present a simple two-dimensional dynamical system where two nonlinear terms, exerting respectively positive feedback and reversal, compete to create a singularity in finite time decorated by accelerating oscillations. The power law singularity results from the increasing growth rate. The oscillations result from the restoring mechanism. As a function of the order of the nonlinearity of the growth rate and of the restoring term, a rich variety of behavior is documented analytically and numerically. The dynamical behavior is traced back fundamentally to the self-similar spiral structure of trajectories in phase space unfolding around an unstable spiral point at the origin. The interplay between the restoring mechanism and the nonlinear growth rate leads to approximately log-periodic oscillations with remarkable scaling properties. Three domains of applications are discussed: (1) the stock market with a competition between nonlinear trend-followers and nonlinear value investors; (2) the world human population with a competition between a population-dependent growth rate and a nonlinear dependence on a finite carrying capacity; (3) the failure of a material subjected to a time-varying stress with a competition between positive geometrical feedback on the damage variable and nonlinear healing.Comment: Latex document of 59 pages including 20 eps figure

Classification of Possible Finite-Time Singularities by Functional Renormalization

Starting from a representation of the early time evolution of a dynamical system in terms of the polynomial expression of some observable f (t) as a function of the time variable in some interval 0 < t < T, we investigate how to extrapolate/forecast in some optimal stability sense the future evolution of f(t) for time t>T. Using the functional renormalization of Yukalov and Gluzman, we offer a general classification of the possible regimes that can be defined based on the sole knowledge of the coefficients of a second-order polynomial representation of the dynamics. In particular, we investigate the conditions for the occurence of finite-time singularities from the structure of the time series, and quantify the critical time and the functional nature of the singularity when present. We also describe the regimes when a smooth extremum replaces the singularity and determine its position and amplitude. This extends previous works by (1) quantifying the stability of the functional renormalization method more accurately, (2) introducing new global constraints in terms of moments and (3) going beyond the ``mean-field'' approximation.Comment: Latex document of 18 pages + 7 ps figure

How are podocytes affected in nail–patella syndrome?

Nail–patella syndrome is an autosomal-dominant hereditary disease named for dysplastic fingernails and toenails and hypoplastic or absent kneecaps evident in patients with the syndrome. Prognosis is determined by the nephropathy that develops in many such patients. Besides podocyte foot-process effacement, pathognomonic changes in the kidney comprise electron-lucent areas and fibrillar inclusions in the glomerular basement membrane. These characteristic symptoms are caused by mutations in the gene encoding the transcription factor LMX1B, a member of the LIM-homeodomain gene family. Comparable with the human syndrome, homozygous Lmx1b knockout mice lack patellae and suffer from severe podocyte damage. In contrast, however, podocin and the α3 and α4 chains of collagen IV are absent in the glomeruli of Lmx1b knockout mice. Further studies with podocyte-specific Lmx1b knockout mice have confirmed the importance of LMX1B in podocytes, as these mice apparently develop foot processes initially but lose them later on. We therefore conclude that LMX1B is essential for the development of metanephric precursor cells into podocytes and possibly also for maintaining the differentiation status of podocytes. LMX1B can serve as a model system to elucidate a genetic program in podocytes

Genomic analysis of the necrotrophic fungal pathogens Sclerotinia sclerotiorum and Botrytis cinerea

This is the final version of the article. Available from the publisher via the DOI in this record.Sclerotinia sclerotiorum and Botrytis cinerea are closely related necrotrophic plant pathogenic fungi notable for their wide host ranges and environmental persistence. These attributes have made these species models for understanding the complexity of necrotrophic, broad host-range pathogenicity. Despite their similarities, the two species differ in mating behaviour and the ability to produce asexual spores. We have sequenced the genomes of one strain of S. sclerotiorum and two strains of B. cinerea. The comparative analysis of these genomes relative to one another and to other sequenced fungal genomes is provided here. Their 38-39 Mb genomes include 11,860-14,270 predicted genes, which share 83% amino acid identity on average between the two species. We have mapped the S. sclerotiorum assembly to 16 chromosomes and found large-scale co-linearity with the B. cinerea genomes. Seven percent of the S. sclerotiorum genome comprises transposable elements compared to <1% of B. cinerea. The arsenal of genes associated with necrotrophic processes is similar between the species, including genes involved in plant cell wall degradation and oxalic acid production. Analysis of secondary metabolism gene clusters revealed an expansion in number and diversity of B. cinerea-specific secondary metabolites relative to S. sclerotiorum. The potential diversity in secondary metabolism might be involved in adaptation to specific ecological niches. Comparative genome analysis revealed the basis of differing sexual mating compatibility systems between S. sclerotiorum and B. cinerea. The organization of the mating-type loci differs, and their structures provide evidence for the evolution of heterothallism from homothallism. These data shed light on the evolutionary and mechanistic bases of the genetically complex traits of necrotrophic pathogenicity and sexual mating. This resource should facilitate the functional studies designed to better understand what makes these fungi such successful and persistent pathogens of agronomic crops.The Sclerotinia sclerotiorum genome project was supported by the USDA Cooperative State Research, Education and Extension Service (USDA-NRI 2004). Sclerotinia sclerotiorum ESTs were funded by a grant to JA Rollins from USDA specific cooperative agreement 58-5442-4-281. The genome sequence of Botrytis cinerea strain T4 was funded by Genoscope, CEA, France. M Viaud was funded by the “Projet INRA Jeune-Equipe”. PM Coutinho and B Henrissat were funded by the ANR to project E-Tricel (grant ANR-07-BIOE-006). The CAZy database is funded in part by GIS-IBiSA. DM Soanes and NJ Talbot were partly funded by the UK Biotechnology and Biological Sciences Research Council. KM Plummer was partially funded by the New Zealand Bio-Protection Research Centre, http://bioprotection.org.nz/. BJ Howlett and A Sexton were partially funded by the Australian Grains Research and Development Corporation, www.grdc.com.au. L Kohn was partially funded by NSERC Discovery Grant (Natural Sciences and Engineering Research Council of Canada) - Grant number 458078. M Dickman was supported by the NSF grant MCB-092391 and BARD grant US-4041-07C. O Yarden was supported by BARD grant US-4041-07C. EG Danchin obtained financial support from the European Commission (STREP FungWall grant, contract: LSHB - CT- 2004 - 511952). A Botrytis Genome Workshop (Kaiserslautern, Germany) was supported by a grant from the German Science Foundation (DFG; HA1486) to M Hahn

A recent increase in global wave power as a consequence of oceanic warming

Wind-generated ocean waves drive important coastal processes that determine flooding and erosion. Ocean warming has been one factor affecting waves globally. Most studies have focused on studying parameters such as wave heights, but a systematic, global and long-term signal of climate change in global wave behavior remains undetermined. Here we show that the global wave power, which is the transport of the energy transferred from the wind into sea-surface motion, has increased globally (0.4% per year) and by ocean basins since 1948. We also find long-term correlations and statistical dependency with sea surface temperatures, globally and by ocean sub-basins, particularly between the tropical Atlantic temperatures and the wave power in high south latitudes, the most energetic region globally. Results indicate the upper-ocean warming, a consequence of anthropogenic global warming, is changing the global wave climate, making waves stronger. This identifies wave power as a potentially valuable climate change indicator.Funding for this project was partly provided by RISKOADAPT (BIA2017-89401-R) Spanish Ministry of Science, Innovation and Universities and the ECLISEA project part of the Horizon 2020 ERANET ERA4CS (European Research Area for Climate Services) 2016 Call

Histone deacetylase inhibitors: potential targets responsible for their anti-cancer effect

The histone deacetylase inhibitors (HDACi) have demonstrated anticancer efficacy across a range of malignancies, most impressively in the hematological cancers. It is uncertain whether this clinical efficacy is attributable predominantly to their ability to induce apoptosis and differentiation in the cancer cell, or to their ability to prime the cell to other pro-death stimuli such as those from the immune system. HDACi-induced apoptosis occurs through altered expression of genes encoding proteins in both intrinsic and extrinsic apoptotic pathways; through effects on the proteasome/aggresome systems; through the production of reactive oxygen species, possibly by directly inducing DNA damage; and through alterations in the tumor microenvironment. In addition HDACi increase the immunogenicity of tumor cells and modulate cytokine signaling and potentially T-cell polarization in ways that may contribute the anti-cancer effect in vivo. Here, we provide an overview of current thinking on the mechanisms of HDACi activity, with attention given to the hematological malignancies as well as scientific observations arising from the clinical trials. We also focus on the immune effects of these agents