Modeling seismic wave propagation and amplification in 1D/2D/3D linear and nonlinear unbounded media

To analyze seismic wave propagation in geological structures, it is possible to consider various numerical approaches: the finite difference method, the spectral element method, the boundary element method, the finite element method, the finite volume method, etc. All these methods have various advantages and drawbacks. The amplification of seismic waves in surface soil layers is mainly due to the velocity contrast between these layers and, possibly, to topographic effects around crests and hills. The influence of the geometry of alluvial basins on the amplification process is also know to be large. Nevertheless, strong heterogeneities and complex geometries are not easy to take into account with all numerical methods. 2D/3D models are needed in many situations and the efficiency/accuracy of the numerical methods in such cases is in question. Furthermore, the radiation conditions at infinity are not easy to handle with finite differences or finite/spectral elements whereas it is explicitely accounted in the Boundary Element Method. Various absorbing layer methods (e.g. F-PML, M-PML) were recently proposed to attenuate the spurious wave reflections especially in some difficult cases such as shallow numerical models or grazing incidences. Finally, strong earthquakes involve nonlinear effects in surficial soil layers. To model strong ground motion, it is thus necessary to consider the nonlinear dynamic behaviour of soils and simultaneously investigate seismic wave propagation in complex 2D/3D geological structures! Recent advances in numerical formulations and constitutive models in such complex situations are presented and discussed in this paper. A crucial issue is the availability of the field/laboratory data to feed and validate such models.Comment: of International Journal Geomechanics (2010) 1-1

A Simplified Elastic Model for Seismic Analysis of Earth-Retaining Structures with Limited Displacements

A simplified elastic model for analyzing static and dynamic interaction between earth-retaining structures and backfill within the range of small displacements is presented. The postulated model covers some of the available models as special cases. The model lends itself readily to the treatment of non-homogeneous backfills with elastic properties varying with depth. Internal (linear) damping in the backfill can be included without impairing the simplicity of the model. Radiation losses due to waves propagating horizontally in fills of semi-infinite extent are inherent to the postulated model. The solutions for some statical and dynamical problems of practical importance show satisfactory agreement with results based on the classical theory of elasticity

Nucleation of rupture under slip dependent friction law: Simple models of fault zone

The initiation of frictional instability is investigated for simple models of fault zone using a linearized perturbation analysis. The fault interface is assumed to obey a linear slip-weakening law. The fault is initially prestressed uniformly at the sliding threshold. In the case of antiplane shear between two homogeneous linearly elastic media, space-time and spectral solutions are obtained and shown to be consistent. The nucleation is characterized by (1) a long-wavelength unstable spectrum bounded by a critical wave number; (2) an exponential growth of the unstable modes; and (3) an induced off-fault deformation that remains trapped within a bounded zone in the vicinity of the fault. These phenomena are characterized in terms of the elastic parameters of the surrounding medium and a nucleation length that results from the coupling between the frictional interface and the bulk elasticity. These results are extended to other geometries within the same formalism and implications for three-dimensional rupture are discussed. Finally, internal fault structures are investigated in terms of a fault-parallel damaged zone. Spectral solutions are obtained for both a smooth and a layered distribution of damage. For natural faults the nucleation is shown to depend strongly on the existence of a internal damaged layer. This nucleation can be described in terms of an effective homogeneous model. In all cases, frictional trapping of the deformation out of the fault can lead to the property that arbitrarily long wavelengths remain sensitive to the existence of a fault zone

Atenuación de ondas elásticas con barreras de pilotes

Se presenta una solución analítica para resolver el problema de aislamiento de cimentaciones, de vibraciones generadas en su cercanía, mediante barreras de pilotes. El sistema de aislamiento está formado por una línea de pilotes elásticos y la exitación está dada por una fuente de ondas cilíndricas SV. El problema se formula bidimensionalmente como uno de difracción múltiple de ondas elásticas, los campos reflejados y refractados por los pilotes se construyen mediante expansiones de funciones de ondas cilíndricas. La solución exacta se obtiene al satisfacer idénticamente las condiciones de continuidad de desplazamientos y esfuerzos en las interfases suelo-pilote, con la ayuda del teorema de adición de Graf. Se presentan algunos resultados numéricos que muestran el comportamiento de barreras de pilotes como sistema de aislamiento, y se define un índice de transmisibilidad para medir su efectividad

An algorithm to obtain global solutions of the double confluent Heun equation

A procedure is proposed to construct solutions of the double confluent Heun equation with a determinate behaviour at the singular points. The connection factors are expressed as quotients of Wronskians of the involved solutions. Asymptotic expansions are used in the computation of those Wronskians. The feasibility of the method is shown in an example, namely, the Schroedinger equation with a quasi-exactly-solvable potential

Topoisomerase II inhibitors induce DNA damage-dependent interferon responses circumventing Ebola virus immune evasion

Ebola virus (EBOV) protein VP35 inhibits production of interferon alpha/beta (IFN) by blocking RIG-I-like receptor signaling pathways, thereby promoting virus replication and pathogenesis. A high-throughput screening assay, developed to identify compounds that either inhibit or bypass VP35 IFN-antagonist function, identified five DNA intercalators as reproducible hits from a library of bioactive compounds. Four, including doxorubicin and daunorubicin, are anthracycline antibiotics that inhibit topoisomerase II and are used clinically as chemotherapeutic drugs. These compounds were demonstrated to induce IFN responses in an ATM kinase-dependent manner and to also trigger the DNA-sensing cGAS-STING pathway of IFN induction. These compounds also suppress EBOV replication in vitro and induce IFN in the presence of IFN-antagonist proteins from multiple negative-sense RNA viruses. These findings provide new insights into signaling pathways activated by important chemotherapy drugs and identify a novel therapeutic approach for IFN induction that may be exploited to inhibit RNA virus replication

Cloning and heterologous expression of Lactobacillus reuteri uroporphyrinogen III synthase/methyltransferase gene (cobA/hemD): Preliminary characterization

Some strains of Lb. reuteri produce cobalamin (vitamin B12). Cobalamin biosynthesis relies on the sequential action of more than 25 enzymes in a complex metabolic pathway. We have cloned, expressed and characterized the gene in Lb. reuteri that codes for the S-adenosy L-methionine uroprophyrinogen III methyltransferase/synthase (CobA/HemD), a key bifunctional enzyme in the biosynthesis of cobalamin and other tetrapyrrols.Fil: Vannini, María Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; ArgentinaFil: Rodríguez, Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; ArgentinaFil: Vera, José Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; ArgentinaFil: de Valdéz, Graciela F.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Taranto, Maria Pia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; ArgentinaFil: Sesma, Fernando Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentin

Dengue virus co-opts UBR4 to degrade STAT2 and antagonize type I interferon signaling.

An estimated 50 million dengue virus (DENV) infections occur annually and more than forty percent of the human population is currently at risk of developing dengue fever (DF) or dengue hemorrhagic fever (DHF). Despite the prevalence and potential severity of DF and DHF, there are no approved vaccines or antiviral therapeutics available. An improved understanding of DENV immune evasion is pivotal for the rational development of anti-DENV therapeutics. Antagonism of type I interferon (IFN-I) signaling is a crucial mechanism of DENV immune evasion. DENV NS5 protein inhibits IFN-I signaling by mediating proteasome-dependent STAT2 degradation. Only proteolytically-processed NS5 can efficiently mediate STAT2 degradation, though both unprocessed and processed NS5 bind STAT2. Here we identify UBR4, a 600-kDa member of the N-recognin family, as an interacting partner of DENV NS5 that preferentially binds to processed NS5. Our results also demonstrate that DENV NS5 bridges STAT2 and UBR4. Furthermore, we show that UBR4 promotes DENV-mediated STAT2 degradation, and most importantly, that UBR4 is necessary for efficient viral replication in IFN-I competent cells. Our data underscore the importance of NS5-mediated STAT2 degradation in DENV replication and identify UBR4 as a host protein that is specifically exploited by DENV to inhibit IFN-I signaling via STAT2 degradation