A Robust Solver for a Second Order Mixed Finite Element Method for the Cahn-Hilliard Equation

We develop a robust solver for a second order mixed finite element splitting scheme for the Cahn-Hilliard equation. This work is an extension of our previous work in which we developed a robust solver for a first order mixed finite element splitting scheme for the Cahn-Hilliard equaion. The key ingredient of the solver is a preconditioned minimal residual algorithm (with a multigrid preconditioner) whose performance is independent of the spacial mesh size and the time step size for a given interfacial width parameter. The dependence on the interfacial width parameter is also mild.Comment: 17 pages, 3 figures, 4 tables. arXiv admin note: substantial text overlap with arXiv:1709.0400

A robust solver for a second order mixed finite element method for the Cahn–Hilliard equation

We develop a robust solver for a second order mixed finite element splitting scheme for the Cahn–Hilliard equation. This work is an extension of our previous work in which we developed a robust solver for a first order mixed finite element splitting scheme for the Cahn–Hilliard equation. The key ingredient of the solver is a preconditioned minimal residual algorithm (with a multigrid preconditioner) whose performance is independent of the spatial mesh size and the time step size for a given interfacial width parameter. The dependence on the interfacial width parameter is also mild

Integrating ecology and technology to create innovative pest control devices

Blackie, H., MacMorran, D., Shapiro, L., Woodhead, I., Diegel, O., Murphy, E., Eason, C.T

Lrp5 and Lrp6 exert overlapping functions in osteoblasts during postnatal bone acquisition

The canonical Wnt signaling pathway is critical for skeletal development and maintenance, but the precise roles of the individual Wnt co-receptors, Lrp5 and Lrp6, that enable Wnt signals to be transmitted in osteoblasts remain controversial. In these studies, we used Cre-loxP recombination, in which Cre-expression is driven by the human osteocalcin promoter, to determine the individual contributions of Lrp5 and Lrp6 in postnatal bone acquisition and osteoblast function. Mice selectively lacking either Lrp5 or Lrp6 in mature osteoblasts were born at the expected Mendelian frequency but demonstrated significant reductions in whole-body bone mineral density. Bone architecture measured by microCT revealed that Lrp6 mutant mice failed to accumulate normal amounts of trabecular bone. By contrast, Lrp5 mutants had normal trabecular bone volume at 8 weeks of age, but with age, these mice also exhibited trabecular bone loss. Both mutants also exhibited significant alterations in cortical bone structure. In vitro differentiation was impaired in both Lrp5 and Lrp6 null osteoblasts as indexed by alkaline phosphatase and Alizarin red staining, but the defect was more pronounced in Lrp6 mutant cells. Mice lacking both Wnt co-receptors developed severe osteopenia similar to that observed previously in mice lacking β-catenin in osteoblasts. Likewise, calvarial cells doubly deficient for Lrp5 and Lrp6 failed to form osteoblasts when cultured in osteogenic media, but instead attained a chondrocyte-like phenotype. These results indicate that expression of both Lrp5 and Lrp6 are required within mature osteoblasts for normal postnatal bone development

Transverse Domain Wall Profile for Spin Logic Applications

Domain wall (DW) based logic and memory devices require precise control and manipulation of DW in nanowire conduits. The topological defects of Transverse DWs (TDW) are of paramount importance as regards to the deterministic pinning and movement of DW within complex networks of conduits. In-situ control of the DW topological defects in nanowire conduits may pave the way for novel DW logic applications. In this work, we present a geometrical modulation along a nanowire conduit, which allows for the topological rectification/inversion of TDW in nanowires. This is achieved by exploiting the controlled relaxation of the TDW within an angled rectangle. Direct evidence of the logical operation is obtained via magnetic force microscopy measurement

A genetic algorithm for the one-dimensional cutting stock problem with setups

This paper investigates the one-dimensional cutting stock problem considering two conflicting objective functions: minimization of both the number of objects and the number of different cutting patterns used. A new heuristic method based on the concepts of genetic algorithms is proposed to solve the problem. This heuristic is empirically analyzed by solving randomly generated instances and also practical instances from a chemical-fiber company. The computational results show that the method is efficient and obtains positive results when compared to other methods from the literature. © 2014 Brazilian Operations Research Society

An osteocalcin-deficient mouse strain without endocrine abnormalities

Osteocalcin (OCN), the most abundant noncollagenous protein in the bone matrix, is reported to be a bone-derived endocrine hormone with wide-ranging effects on many aspects of physiology, including glucose metabolism and male fertility. Many of these observations were made using an OCN-deficient mouse allele (Osc– ) in which the 2 OCN-encoding genes in mice, Bglap and Bglap2, were deleted in ES cells by homologous recombination. Here we describe mice with a new Bglap and Bglap2 double-knockout (dko) allele (Bglap/2p.Pro25fs17Ter) that was generated by CRISPR/Cas9-mediated gene editing. Mice homozygous for this new allele do not express full-length Bglap or Bglap2 mRNA and have no immunodetectable OCN in their serum. FTIR imaging of cortical bone in these homozygous knockout animals finds alterations in the collagen maturity and carbonate to phosphate ratio in the cortical bone, compared with wild-type littermates. However, μCT and 3-point bending tests do not find differences from wild-type littermates with respect to bone mass and strength. In contrast to the previously reported OCN-deficient mice with the Osc− allele, serum glucose levels and male fertility in the OCN-deficient mice with the Bglap/ 2pPro25fs17Ter allele did not have significant differences from wild-type littermates. We cannot explain the absence of endocrine effects in mice with this new knockout allele. Possible explanations include the effects of each mutated allele on the transcription of neighboring genes, or differences in genetic background and environment. So that our findings can be confirmed and extended by other interested investigators, we are donating this new Bglap and Bglap2 double-knockout strain to the Jackson Laboratories for academic distribution

The accessible chromatin landscape of the human genome

DNaseI hypersensitive sites (DHSs) are markers of regulatory DNA and have underpinned the discovery of all classes of cis-regulatory elements including enhancers, promoters, insulators, silencers, and locus control regions. Here we present the first extensive map of human DHSs identified through genome-wide profiling in 125 diverse cell and tissue types. We identify ~2.9 million DHSs that encompass virtually all known experimentally-validated cis-regulatory sequences and expose a vast trove of novel elements, most with highly cell-selective regulation. Annotating these elements using ENCODE data reveals novel relationships between chromatin accessibility, transcription, DNA methylation, and regulatory factor occupancy patterns. We connect ~580,000 distal DHSs with their target promoters, revealing systematic pairing of different classes of distal DHSs and specific promoter types. Patterning of chromatin accessibility at many regulatory regions is choreographed with dozens to hundreds of co-activated elements, and the trans-cellular DNaseI sensitivity pattern at a given region can predict cell type-specific functional behaviors. The DHS landscape shows signatures of recent functional evolutionary constraint. However, the DHS compartment in pluripotent and immortalized cells exhibits higher mutation rates than that in highly differentiated cells, exposing an unexpected link between chromatin accessibility, proliferative potential and patterns of human variation

Author Correction: Expanded encyclopaedias of DNA elements in the human and mouse genomes

Online Correction for: https://doi.org/10.1038/s41586-020-2493-4 | Erratum for https://bura.brunel.ac.uk/handle/2438/21299In the version of this article initially published, two members of the ENCODE Project Consortium were missing from the author list. Rizi Ai (Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA, USA) and Shantao Li (Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT, USA) are now included in the author list. These errors have been corrected in the online version of the article : 'Expanded encyclopaedias of DNA elements in the human and mouse genomes'.https://www.nature.com/articles/s41586-021-04226-3https://www.nature.com/articles/s41586-021-04226-