Genetic programming for fiber-threading for fiber-reinforced plastics

Setting up fiber-threading for a pultrusion line is tedious, error prone and takes a long time. Between 100 and 1000 fibers have to be arranged into a two-dimensional shape, which have to be threaded between several support plates without causing crossovers. When manually planning this process based on intuition, it is hard to keep track of the complexity. This slows the process down to where it can take several hours or several days, and shortening this duration reduces the cost considerably. As planning the setup takes up a large chunk of time, we are proposing a simulation and an algorithm to automatically calculate how the fiber bundles need to be threaded from the creels through the support plates to result in the desired shape. Using a three-dimensional simulation for collision detection in conjunction with a genetic algorithm, we are able to shorten the planning of the fibers to around 10 minutes on a modern 8-core personal computer. Based on this data, further work can be done to further improve, visualize or permanently store the data in a digitized company

Collins and Sivers asymmetries in muonproduction of pions and kaons off transversely polarised protons

Measurements of the Collins and Sivers asymmetries for charged pions and charged and neutral kaons produced in semi-inclusive deep-inelastic scattering of high energy muons off transversely polarised protons are presented. The results were obtained using all the available COMPASS proton data, which were taken in the years 2007 and 2010. The Collins asymmetries exhibit in the valence region a non-zero signal for pions and there are hints of non-zero signal also for kaons. The Sivers asymmetries are found to be positive for positive pions and kaons and compatible with zero otherwise. © 2015

A real-word realization of the AntNet routing algorithm with ActivityBots

To ease teaching self-organizing systems design, we implemented the AntNet routing algorithm for real-world application using educational robots called ActivityBot. Using line sensors and ultrasonic distance sensors, the robotic ants traverse a tiled graph printed on paper, collectively converging to the shortest path. In our descriptions, we address the challenges to face when employing such self-organizing systems on educational hardware and provide a video on YouTube https://youtu.be/JFduHJ0o0UM

Effect of macrophage overexpression of murine liver X receptor-alpha (LXR-alpha) on atherosclerosis in LDL-receptor deficient mice

Background- The nuclear liver X receptor-alpha (LXR-alpha) has been implicated in the regulation of intracellular cholesterol homeostasis, inflammatory response, and atherosclerosis susceptibility. The aim of the present study was to test whether transgenic expression of LXR-alpha might affect these mechanisms and result in a reduction of atherosclerosis. METHODS AND RESULTS: We generated mice with macrophage overexpression of mouse LXR-alpha, evidenced by significantly elevated expression levels of LXR-target genes (ABCA1, ABCG1) in these cells. For atherosclerosis studies, mice were crossed onto the LDL-receptor deficient background. Plasma lipids and lipoproteins as well as liver triglycerides were not significantly different between transgenic animals and nontransgenic controls. However, lesion area at the brachiocephalic artery (BCA) was significantly reduced (-83%, P=0.02) in male LXR-alpha transgenic mice. This was associated with a significantly increased cholesterol efflux to acceptor-free media (+24%, P=0.002) and ApoA1 containing media (+20%, P<0.0001) as well as reduced lipopolysaccharide (LPS)-induced NO-release from macrophages of transgenic animals, providing a potential mechanism for the reduction of atherosclerosis. CONCLUSIONS: Our data show for the first time that transgenic overexpression of LXR-alpha in macrophages has significant antiatherogenic properties. We conclude that overexpression of LXR-alpha in macrophages might be useful as a therapeutic principle for the prevention of atherosclerosis

Circular non-coding RNA ANRIL modulates ribosomal RNA maturation and atherosclerosis in humans

Circular RNAs (circRNAs) are broadly expressed in eukaryotic cells, but their molecular mechanism in human disease remains obscure. Here we show that circular antisense non-coding RNA in the INK4 locus (circANRIL), which is transcribed at a locus of atherosclerotic cardiovascular disease on chromosome 9p21, confers atheroprotection by controlling ribosomal RNA (rRNA) maturation and modulating pathways of atherogenesis. CircANRIL binds to pescadillo homologue 1 (PES1), an essential 60S-preribosomal assembly factor, thereby impairing exonuclease-mediated pre-rRNA processing and ribosome biogenesis in vascular smooth muscle cells and macrophages. As a consequence, circANRIL induces nucleolar stress and p53 activation, resulting in the induction of apoptosis and inhibition of proliferation, which are key cell functions in atherosclerosis. Collectively, these findings identify circANRIL as a prototype of a circRNA regulating ribosome biogenesis and conferring atheroprotection, thereby showing that circularization of long non-coding RNAs may alter RNA function and protect from human disease

Alu Elements in <i>ANRIL</i> Non-Coding RNA at Chromosome 9p21 Modulate Atherogenic Cell Functions through <i>Trans</i>-Regulation of Gene Networks

<div><p>The chromosome 9p21 (Chr9p21) locus of coronary artery disease has been identified in the first surge of genome-wide association and is the strongest genetic factor of atherosclerosis known today. Chr9p21 encodes the long non-coding RNA (ncRNA) <i>antisense non-coding RNA in the INK4 locus</i> (<i>ANRIL</i>). <i>ANRIL</i> expression is associated with the Chr9p21 genotype and correlated with atherosclerosis severity. Here, we report on the molecular mechanisms through which <i>ANRIL</i> regulates target-genes <i>in trans</i>, leading to increased cell proliferation, increased cell adhesion and decreased apoptosis, which are all essential mechanisms of atherogenesis. Importantly, <i>trans</i>-regulation was dependent on Alu motifs, which marked the promoters of <i>ANRIL</i> target genes and were mirrored in <i>ANRIL</i> RNA transcripts. <i>ANRIL</i> bound Polycomb group proteins that were highly enriched in the proximity of Alu motifs across the genome and were recruited to promoters of target genes upon <i>ANRIL</i> over-expression. The functional relevance of Alu motifs in <i>ANRIL</i> was confirmed by deletion and mutagenesis, reversing <i>trans</i>-regulation and atherogenic cell functions. <i>ANRIL</i>-regulated networks were confirmed in 2280 individuals with and without coronary artery disease and functionally validated in primary cells from patients carrying the Chr9p21 risk allele. Our study provides a molecular mechanism for pro-atherogenic effects of <i>ANRIL</i> at Chr9p21 and suggests a novel role for Alu elements in epigenetic gene regulation by long ncRNAs.</p></div