3D mesh refinement procedure using the bisection and rivara algorithms with mesh quality assessment

Mesh refinement procedures for the solution of three dimensional problems are described. The computational\ud domain is represented by an assembly of tetrahedral elements and the mesh refinement is acheived by the bisection\ud and Rivara methods using an explicit mesh density function coupled with an automatic 3D mesh generator.\ud A couple of benchmark examples is used to compare the performance of both refinement methods in terms of mesh\ud and size qualities, number of generated elements and CPU time consume

P-Selectivity, Immunity, and the Power of One Bit

We prove that P-sel, the class of all P-selective sets, is EXP-immune, but is not EXP/1-immune. That is, we prove that some infinite P-selective set has no infinite EXP-time subset, but we also prove that every infinite P-selective set has some infinite subset in EXP/1. Informally put, the immunity of P-sel is so fragile that it is pierced by a single bit of information. The above claims follow from broader results that we obtain about the immunity of the P-selective sets. In particular, we prove that for every recursive function f, P-sel is DTIME(f)-immune. Yet we also prove that P-sel is not \Pi_2^p/1-immune

Proteostasis and ageing: insights from long-lived mutant mice

The global increase in life expectancy is creating significant medical, social and economic challenges to current and future generations. Consequently, there is a need to identify the fundamental mechanisms underlying the ageing process. This knowledge should help develop realistic interventions capable of combatting age-related disease, and thus improving late-life health and vitality. While several mechanisms have been proposed as conserved lifespan determinants, the loss of proteostasis- where proteostasis is defined here as the maintenance of the proteome- appears highly relevant to both ageing and disease. Several studies have shown that multiple proteostatic mechanisms, including the endoplasmic reticulum (ER)-induced unfolded protein response (UPR), the ubiquitin-proteasome system (UPS) and autophagy, all appear indispensable for longevity in many long-lived invertebrate mutants. Similarly, interspecific comparisons suggest that proteostasis may be an important lifespan determinant in vertebrates. Over the last 20 years a number of long-lived mouse mutants have been described, many of which carry single-gene mutations within the growth-hormone, insulin/IGF-1 or mTOR signalling pathways. However, we still do not know how these mutations act mechanistically to increase lifespan and healthspan, and accordingly whether mechanistic commonality occurs between different mutants. Recent evidence supports the premise that the successful maintenance of the proteome during ageing may be linked to the increased lifespan and healthspan of long-lived mouse mutants

Wrinkling prediction with adaptive mesh refinement

An adaptive mesh refinement procedure for wrinkling prediction analyses is presented. First the\ud critical values are determined using Hutchinson’s bifurcation functional. A wrinkling risk factor is then\ud defined and used to determined areas of potential wrinkling risk. Finally, a mesh refinement is operate

Chronic helminth infection burden differentially affects haematopoietic cell development while ageing selectively impairs adaptive responses to infection

Throughout the lifespan of an individual, the immune system undergoes complex changes while facing novel and chronic infections. Helminths, which infect over one billion people and impose heavy livestock productivity losses, typically cause chronic infections by avoiding and suppressing host immunity. Yet, how age affects immune responses to lifelong parasitic infection is poorly understood. To disentangle the processes involved, we employed supervised statistical learning techniques to identify which factors among haematopoietic stem and progenitor cells (HSPC), and both innate and adaptive responses regulate parasite burdens and how they are affected by host age. Older mice harboured greater numbers of the parasites’ offspring than younger mice. Protective immune responses that did not vary with age were dominated by HSPC, while ageing specifically eroded adaptive immunity, with reduced numbers of naïve T cells, poor T cell responsiveness to parasites, and impaired antibody production. We identified immune factors consistent with previously-reported immune responses to helminths, and also revealed novel interactions between helminths and HSPC maturation. Our approach thus allowed disentangling the concurrent effects of ageing and infection across the full maturation cycle of the immune response and highlights the potential of such approaches to improve understanding of the immune system within the whole organism