4 resultados para DAMAGE EVOLUTION TRACKING

em CentAUR: Central Archive University of Reading - UK


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We present results on the growth of damage in 29 fatigue tests of human femoral cortical bone from four individuals, aged 53–79. In these tests we examine the interdependency of stress, cycles to failure, rate of creep strain, and rate of modulus loss. The behavior of creep rates has been reported recently for the same donors as an effect of stress and cycles (Cotton, J. R., Zioupos, P., Winwood, K., and Taylor, M., 2003, "Analysis of Creep Strain During Tensile Fatigue of Cortical Bone," J. Biomech. 36, pp. 943–949). In the present paper we first examine how the evolution of damage (drop in modulus per cycle) is associated with the stress level or the "normalized stress" level (stress divided by specimen modulus), and results show the rate of modulus loss fits better as a function of normalized stress. However, we find here that even better correlations can be established between either the cycles to failure or creep rates versus rates of damage than any of these three measures versus normalized stress. The data indicate that damage rates can be excellent predictors of fatigue life and creep strain rates in tensile fatigue of human cortical bone for use in practical problems and computer simulations.

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The immense social and economic impact of bacterial pathogens, from drug-resistant infections in hospitals to the devastation of agricultural resources, has resulted in major investment to understand the causes and conse- quences of pathogen evolution. Recent genome se- quencing projects have provided insight into the evolution of bacterial genome structures; revealing the impact of mobile DNA on genome restructuring and pathogenicity. Sequencing of multiple genomes of relat- ed strains has enabled the delineation of pathogen evo- lution and facilitated the tracking of bacterial pathogens globally. Other recent theoretical and empirical studies have shown that pathogen evolution is significantly influenced by ecological factors, such as the distribution of hosts within the environment and the effects of co- infection. We suggest that the time is ripe for experi- mentalists to use genomics in conjunction with evolu- tionary ecology experiments to further understanding of how bacterial pathogens evolve.

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The synoptic evolution and some meteorological impacts of the European winter storm Kyrill that swept across Western, Central, and Eastern Europe between 17 and 19 January 2007 are investigated. The intensity and large storm damage associated with Kyrill is explained based on synoptic and mesoscale environmental storm features, as well as on comparisons to previous storms. Kyrill appeared on weather maps over the US state of Arkansas about four days before it hit Europe. It underwent an explosive intensification over the Western North Atlantic Ocean while crossing a very intense zonal polar jet stream. A superposition of several favourable meteorological conditions west of the British Isles caused a further deepening of the storm when it started to affect Western Europe. Evidence is provided that a favourable alignment of three polar jet streaks and a dry air intrusion over the occlusion and cold fronts were causal factors in maintaining Kyrill's low pressure very far into Eastern Europe. Kyrill, like many other strong European winter storms, was embedded in a pre-existing, anomalously wide, north-south mean sea-level pressure (MSLP) gradient field. In addition to the range of gusts that might be expected from the synoptic-scale pressure field, mesoscale features associated with convective overturning at the cold front are suggested as the likely causes for the extremely damaging peak gusts observed at many lowland stations during the passage of Kyrill's cold front. Compared to other storms, Kyrill was by far not the most intense system in terms of core pressure and circulation anomaly. However, the system moved into a pre-existing strong MSLP gradient located over Central Europe which extended into Eastern Europe. This fact is considered determinant for the anomalously large area affected by Kyrill. Additionally, considerations of windiness in climate change simulations using two state-of-the-art regional climate models driven by ECHAM5 indicate that not only Central, but also Eastern Central Europe may be affected by higher surface wind speeds at the end of the 21st century. These changes are partially associated with the increased pressure gradient over Europe which is identified in the ECHAM5 simulations. Thus, with respect to the area affected, as well as to the synoptic and mesoscale storm features, it is proposed that Kyrill may serve as an interesting study case to assess future storm impacts.

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Multicellularity evolved well before 600 million years ago, and all multicellular animals have evolved since then with the need to protect against pathogens. There is no reason to expect their immune systems to be any less sophisticated than ours. The vertebrate system, based on rearranging immunoglobulin-superfamily domains, appears to have evolved partly as a result of chance insertion of RAG genes by horizontal transfer. Remarkably sophisticated systems for expansion of immunological repertoire have evolved in parallel in many groups of organisms. Vaccination of invertebrates against commercially important pathogens has been empirically successful, and suggests that the definition of an adaptive and innate immune system should no longer depend on the presence of memory and specificity, since these terms are hard to define in themselves. The evolution of randomly-created immunological repertoire also carries with it the potential for generating autoreactive specificities and consequent autoimmune damage.While invertebrates may use systems analogous to ours to control autoreactive specificities, they may have evolved alternative mechanisms which operate either at the level of individuals-within-populations rather than cells-within-individuals, by linking self-reactive specificities to regulatory pathways and non-self-reactive to effector pathways.