Multiple SNP Markers Reveal Fine-Scale Population and Deep Phylogeographic Structure in European Anchovy (Engraulis encrasicolus L.)

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“Deborah Numbers”, Coupling Multiple Space and Time Scales and Governing Damage Evolution to Failure

Two different spatial levels are involved concerning damage accumulation to eventual failure. nucleation and growth rates of microdamage nN* and V*. It is found that the trans-scale length ratio c*/L does not directly affect the process. Instead, two independent dimensionless numbers: the trans-scale one * * ( V*)including the * **5 * N c V including mesoscopic parameters only, play the key role in the process of damage accumulation to failure. The above implies that there are three time scales involved in the process: the macroscopic imposed time scale tim = /a and two meso-scopic time scales, nucleation and growth of damage, (* *4) N N t =1 n c and tV=c*/V*. Clearly, the dimensionless number De*=tV/tim refers to the ratio of microdamage growth time scale over the macroscopically imposed time scale. So, analogous to the definition of Deborah number as the ratio of relaxation time over external one in rheology. Let De be the imposed Deborah number while De represents the competition and coupling between the microdamage growth and the macroscopically imposed wave loading. In stress-wave induced tensile failure (spallation) De* < 1, this means that microdamage has enough time to grow during the macroscopic wave loading. Thus, the microdamage growth appears to be the predominate mechanism governing the failure. Moreover, the dimensionless number D* = tV/tN characterizes the ratio of two intrinsic mesoscopic time scales: growth over nucleation. Similarly let D be the “intrinsic Deborah number”. Both time scales are relevant to intrinsic relaxation rather than imposed one. Furthermore, the intrinsic Deborah number D* implies a certain characteristic damage. In particular, it is derived that D* is a proper indicator of macroscopic critical damage to damage localization, like D* ∼ (10–3~10–2) in spallation. More importantly, we found that this small intrinsic Deborah number D* indicates the energy partition of microdamage dissipation over bulk plastic work. This explains why spallation can not be formulated by macroscopic energy criterion and must be treated by multi-scale analysis.

Multiple table factor analysis applied to the higher education competences

Due to the recent implantation of the Bologna process, the definition of competences in Higher Education is an important matter that deserves special attention and requires a detailed analysis. For that reason, we study the importance given to severa! competences for the professional activity and the degree to which these competences have been achieved through the received education. The answers include also competences observed in two periods of time given by individuals of multiple characteristics. In this context and in order to obtain synthesized results, we propose the use of Multiple Table Factor Analysis. Through this analysis, individuals are described by severa! groups, showing the most important variability factors of the individuals and allowing the analysis of the common structure ofthe different data tables. The obtained results will allow us finding out the existence or absence of a common structure in the answers of the various data tables, knowing which competences have similar answer structure in the groups of variables, as well as characterizing those answers through the individuals.

Fine mapping and functional analysis of the multiple sclerosis risk gene CD6

CD6 has recently been identified and validated as risk gene for multiple sclerosis (MS), based on the association of a single nucleotide polymorphism (SNP), rs17824933, located in intron 1. CD6 is a cell surface scavenger receptor involved in T-cell activation and proliferation, as well as in thymocyte differentiation. In this study, we performed a haptag SNP screen of the CD6 gene locus using a total of thirteen tagging SNPs, of which three were non-synonymous SNPs, and replicated the recently reported GWAS SNP rs650258 in a Spanish-Basque collection of 814 controls and 823 cases. Validation of the six most strongly associated SNPs was performed in an independent collection of 2265 MS patients and 2600 healthy controls. We identified association of haplotypes composed of two non-synonymous SNPs [rs11230563 (R225W) and rs2074225 (A257V)] in the 2nd SRCR domain with susceptibility to MS (Pmax(T) permutation=161024). The effect of these haplotypes on CD6 surface expression and cytokine secretion was also tested. The analysis showed significantly different CD6 expression patterns in the distinct cell subsets, i.e. – CD4+ naı¨ve cells, P = 0.0001; CD8+ naı¨ve cells, P,0.0001; CD4+ and CD8+ central memory cells, P = 0.01 and 0.05, respectively; and natural killer T (NKT) cells, P = 0.02; with the protective haplotype (RA) showing higher expression of CD6. However, no significant changes were observed in natural killer (NK) cells, effector memory and terminally differentiated effector memory T cells. Our findings reveal that this new MS-associated CD6 risk haplotype significantly modifies expression of CD6 on CD4+ and CD8+ T cells.