Optimum Design of Thin Wideband Multilayer Electromagnetic Shield Using Evolutionary Algorithms

This paper describes the method of optimum design of multilayer perforated electromagnetic shield using Evolutionary algorithms, namely Particle Swarm Optimization Algorithm (PSO) and Genetic Algorithm (GA). Different parameters which are inherently conflicting in nature corresponds to the multilayer structure of the electromagnetic shields have been considered. The goal is to minimize the overall mass of the shield with respect to its shielding effectiveness and cost. Three different models are considered and synthesized using evolutionary algorithms. Numerical optimal results for each model using different algorithms are presented and compared with each other to establish the effectiveness of the proposed method of designing

Synthesis of Steered Flat-top Beam Pattern Using Evolutionary Algorithm

In this paper a pattern synthesis method based on Evolutionary Algorithm is presented. A Flat-top beam pattern has been generated from a concentric ring array of isotropic elements by finding out the optimum set of elements amplitudes and phases using Differential Evolution algorithm. The said pattern is generated in three predefined azimuth planes instate of a single phi plane and also verified for a range of azimuth plane for the same optimum excitations. The main beam is steered to an elevation angle of 30 degree with lower peak SLL and ripple. Dynamic range ratio (DRR) is also being improved by eliminating the weakly excited array elements, which simplify the design complexity of feed networks

Synthesis of Steered Flat-top Beam Pattern Using Evolutionary Algorithm

In this paper a pattern synthesis method based on Evolutionary Algorithm is presented. A Flat-top beam pattern has been generated from a concentric ring array of isotropic elements by finding out the optimum set of elements amplitudes and phases using Differential Evolution algorithm. The said pattern is generated in three predefined azimuth planes instate of a single phi plane and also verified for a range of azimuth plane for the same optimum excitations. The main beam is steered to an elevation angle of 30 degree with lower peak SLL and ripple. Dynamic range ratio (DRR) is also being improved by eliminating the weakly excited array elements, which simplify the design complexity of feed networks

Engineering self-organising helium bubble lattices in tungsten

The self-organisation of void and gas bubbles in solids into a superlattices is an intriguing nanoscale phenomenon. Despite the discovery of these lattices 30 years ago, the atomistics behind the ordering mechanisms responsible for the formation of these nanostructures are yet to be fully elucidated. Here we report on the direct observation via transmission electron microscopy of the formation of bubble lattices under He+ ion bombardment. By careful control of the irradiation conditions, it has been possible to engineer the bubble size and spacing of the superlattice leading to important conclusions about the significance of vacancy supply in determining the physical characteristics of the system. Furthermore, no bubble lattice alignment was observed in the directions pointing to a key driving mechanism for the formation of these ordered nanostructures being the two-dimensional diffusion of self-interstitial atoms

Dendritic Cells Take up and Present Antigens from Viable and Apoptotic Polymorphonuclear Leukocytes

Dendritic cells (DC) are endowed with the ability to cross-present antigens from other cell types to cognate T cells. DC are poised to meet polymorphonuclear leukocytes (PMNs) as a result of being co-attracted by interleukin-8 (IL-8), for instance as produced by tumor cells or infected tissue. Human monocyte-derived and mouse bone marrow-derived DC can readily internalize viable or UV-irradiated PMNs. Such internalization was abrogated at 4°C and partly inhibited by anti-CD18 mAb. In mice, DC which had internalized PMNs containing electroporated ovalbumin (OVA) protein, were able to cross-present the antigen to CD8 (OT-1) and CD4 (OT-2) TCR-transgenic T cells. Moreover, in humans, tumor cell debris is internalized by PMNs and the tumor-cell material can be subsequently taken up from the immunomagnetically re-isolated PMNs by DC. Importantly, if human neutrophils had endocytosed bacteria, they were able to trigger the maturation program of the DC. Moreover, when mouse PMNs with E. coli in their interior are co-injected in the foot pad with DC, many DC loaded with fluorescent material from the PMNs reach draining lymph nodes. Using CT26 (H-2d) mouse tumor cells, it was observed that if tumor cells are intracellularly loaded with OVA protein and UV-irradiated, they become phagocytic prey of H-2d PMNs. If such PMNs, that cannot present antigens to OT-1 T cells, are immunomagnetically re-isolated and phagocytosed by H-2b DC, such DC productively cross-present OVA antigen determinants to OT-1 T cells. Cross-presentation to adoptively transferred OT-1 lymphocytes at draining lymph nodes also take place when OVA-loaded PMNs (H-2d) are coinjected in the footpad of mice with autologous DC (H-2b). In summary, our results indicate that antigens phagocytosed by short-lived PMNs can be in turn internalized and productively cross-presented by DC

The potential for immunoglobulins and host defense peptides (HDPs) to reduce the use of antibiotics in animal production

Abstract Innate defense mechanisms are aimed at quickly containing and removing infectious microorganisms and involve local stromal and immune cell activation, neutrophil recruitment and activation and the induction of host defense peptides (defensins and cathelicidins), acute phase proteins and complement activation. As an alternative to antibiotics, innate immune mechanisms are highly relevant as they offer rapid general ways to, at least partially, protect against infections and enable the build-up of a sufficient adaptive immune response. This review describes two classes of promising alternatives to antibiotics based on components of the innate host defense. First we describe immunoglobulins applied to mimic the way in which they work in the newborn as locally acting broadly active defense molecules enforcing innate immunity barriers. Secondly, the potential of host defense peptides with different modes of action, used directly, induced in situ or used as vaccine adjuvants is described

Human β-D-3 Exacerbates MDA5 but Suppresses TLR3 Responses to the Viral Molecular Pattern Mimic Polyinosinic:Polycytidylic Acid

Human β-defensin 3 (hBD3) is a cationic host defence peptide and is part of the innate immune response. HBD3 is present on a highly copy number variable block of six β-defensin genes, and increased copy number is associated with the autoimmune disease psoriasis. It is not known how this increase influences disease development, but psoriasis is a T cell-mediated disease and activation of the innate immune system is required for the initial trigger that leads to the amplification stage. We investigated the effect of hBD3 on the response of primary macrophages to various TLR agonists. HBD3 exacerbated the production of type I Interferon-β in response to the viral ligand mimic polyinosinic:polycytidylic acid (polyI:C) in both human and mouse primary cells, although production of the chemokine CXCL10 was suppressed. Compared to polyI:C alone, mice injected with both hBD3 peptide and polyI:C also showed an enhanced increase in Interferon-β. Mice expressing a transgene encoding hBD3 had elevated basal levels of Interferon-β, and challenge with polyI:C further increased this response. HBD3 peptide increased uptake of polyI:C by macrophages, however the cellular response and localisation of polyI:C in cells treated contemporaneously with hBD3 or cationic liposome differed. Immunohistochemistry showed that hBD3 and polyI:C do not co-localise, but in the presence of hBD3 less polyI:C localises to the early endosome. Using bone marrow derived macrophages from knockout mice we demonstrate that hBD3 suppresses the polyI:C-induced TLR3 response mediated by TICAM1 (TRIF), while exacerbating the cytoplasmic response through MDA5 (IFIH1) and MAVS (IPS1/CARDIF). Thus, hBD3, a highly copy number variable gene in human, influences cellular responses to the viral mimic polyI:C implying that copy number may have a significant phenotypic effect on the response to viral infection and development of autoimmunity in humans