Performance Analysis of Tree Seed Algorithm for Small Dimension Optimization Functions

Tree-Seed Algorithm (TSA) simulates the growth of trees and seeds on a land. TSA is a method proposed to solve continuous optimization problems. Trees and seeds indicate possible solutions in the search space for optimization problems. Trees are planted in the ground at the beginning of the search and each tree produces several seeds during iterations. While the trees were selected randomly during seed formation, the tournament selection method was used and also hybridized by adding the C parameter, which is the acceleration coefficient calculated according to the size of the problem. In this study, continuous optimization problem has been solved by the hybrid method. First, the performance analyses of the five best known numerical benchmark functions have been done, in both TSA and hybrid method TSA with 2, 3, 4 and 5 dimensions, and 10-50 population numbers. After that, well-known algorithms in the literature like Particle Swarm Optimization (PSO), TSA, Artificial Bee Colony (ABC), Harmony Search (HS), as well as hybrid method TSA (HTSA) have been applied to twenty-four numerical benchmark functions and the performance analyses of algorithms have been done. Hopeful and comparable conclusions based on solution quality and robustness can be obtained with the hybrid method

A stress free model for residual stress assessment using thermoelastic stress analysis

Thermoelastic Stress Analysis (TSA) has been proposed as a method of obtaining residual stresses. The results of a preliminary study demonstrated that when Al-2024 plate containing holes that were plastically deformed by cold expansion process to 2% and 4% strain the thermoelastic response in the material around the hole was different to that obtained from a plate that had not experienced any plastic cold expansion (i.e. a reference specimen). This observation provides an opportunity for obtaining residual stresses based on TSA data. In many applications a reference specimen (i.e. residual stress free specimen) may not be available for comparison, so a synthetic, digital bitmap has been proposed as an alternative. An elastic finite element model is created using commercially available software Abaqus/Standard and the resultant stress field is extracted. The simulated stress field from the model is mapped onto a grid that matches the TSA pixel data from a physical reference specimen. This stress field is then converted to a ?T/T field that can be compared to the full-field TSA data. When the reference experimental data is subtracted from the, bitmap dataset the resultant ?T/T field is approximately zero. Further work proposes replacing the experimental reference data with that from specimens that have undergone cold expansion with the aim of revealing the regions affected by residual stress through a departure from zero in the resultant stress field. The paper demonstrates the first steps necessary for deriving the residual stresses from a general specimen using TSA

Auxin and epigenetic regulation of SKP2B, an F-box that represses lateral root formation

In plants, lateral roots originate from pericycle founder cells that are specified at regular intervals along the main root. Here, we show that Arabidopsis (Arabidopsis thaliana) SKP2B (for S-Phase Kinase-Associated Protein2B), an F-box protein, negatively regulates cell cycle and lateral root formation as it represses meristematic and founder cell divisions. According to its function, SKP2B is expressed in founder cells, lateral root primordia and the root apical meristem. We identified a novel motif in the SKP2B promoter that is required for its specific root expression and auxin-dependent induction in the pericycle cells. Next to a transcriptional control by auxin, SKP2B expression is regulated by histone H3.1/H3.3 deposition in a CAF-dependent manner. The SKP2B promoter and the 59 end of the transcribed region are enriched in H3.3, which is associated with active chromatin states, over H3.1. Furthermore, the SKP2B promoter is also regulated by H3 acetylation in an auxin-and IAA14-dependent manner, reinforcing the idea that epigenetics represents an important regulatory mechanism during lateral root formation

Human THO–Sin3A interaction reveals new mechanisms to prevent R-loops that cause genome instability

R-loops, formed by co-transcriptional DNA–RNA hybrids and a displaced DNA single strand (ssDNA), fulfill certain positive regulatory roles but are also a source of genomic instability. One key cellular mechanism to prevent R-loop accumulation centers on the conserved THO/TREX complex, an RNA-binding factor involved in transcription elongation and RNA export that contributes to messenger ribonucleoprotein (mRNP) assembly, but whose precise function is still unclear. To understand how THO restrains harmful R-loops, we searched for new THO-interacting factors. We found that human THO interacts with the Sin3A histone deacetylase complex to suppress co-transcriptional R-loops, DNA damage, and replication impairment. Functional analyses show that histone hypo-acetylation prevents accumulation of harmful R-loops and RNA-mediated genomic instability. Diminished histone deacetylase activity in THO- and Sin3A-depleted cell lines correlates with increased R-loop formation, genomic instability, and replication fork stalling. Our study thus uncovers physical and functional crosstalk between RNA-binding factors and chromatin modifiers with a major role in preventing R-loop formation and RNA-mediated genome instability.European Research Council ERC2014 AdG669898 TARLOOPMinisterio de Economía y Competitividad BFU2013-42918-P, BFU2016-75058-PJunta de Andalucía BIO123

An approximation function for frequency constrained structural optimization

The purpose is to examine a function for approximating natural frequency constraints during structural optimization. The nonlinearity of frequencies has posed a barrier to constructing approximations for frequency constraints of high enough quality to facilitate efficient solutions. A new function to represent frequency constraints, called the Rayleigh Quotient Approximation (RQA), is presented. Its ability to represent the actual frequency constraint results in stable convergence with effectively no move limits. The objective of the optimization problem is to minimize structural weight subject to some minimum (or maximum) allowable frequency and perhaps subject to other constraints such as stress, displacement, and gage size, as well. A reason for constraining natural frequencies during design might be to avoid potential resonant frequencies due to machinery or actuators on the structure. Another reason might be to satisy requirements of an aircraft or spacecraft's control law. Whatever the structure supports may be sensitive to a frequency band that must be avoided. Any of these situations or others may require the designer to insure the satisfaction of frequency constraints. A further motivation for considering accurate approximations of natural frequencies is that they are fundamental to dynamic response constraints

Obscurin and KCTD6 regulate cullin-dependent small ankyrin-1 (sAnk1.5) protein turnover.

Protein turnover through cullin-3 is tightly regulated by posttranslational modifications, the COP9 signalosome, and BTB/POZ-domain proteins that link cullin-3 to specific substrates for ubiquitylation. In this paper, we report how potassium channel tetramerization domain containing 6 (KCTD6) represents a novel substrate adaptor for cullin-3, effectively regulating protein levels of the muscle small ankyrin-1 isoform 5 (sAnk1.5). Binding of sAnk1.5 to KCTD6, and its subsequent turnover is regulated through posttranslational modification by nedd8, ubiquitin, and acetylation of C-terminal lysine residues. The presence of the sAnk1.5 binding partner obscurin, and mutation of lysine residues increased sAnk1.5 protein levels, as did knockdown of KCTD6 in cardiomyocytes. Obscurin knockout muscle displayed reduced sAnk1.5 levels and mislocalization of the sAnk1.5/KCTD6 complex. Scaffolding functions of obscurin may therefore prevent activation of the cullin-mediated protein degradation machinery and ubiquitylation of sAnk1.5 through sequestration of sAnk1.5/KCTD6 at the sarcomeric M-band, away from the Z-disk-associated cullin-3. The interaction of KCTD6 with ankyrin-1 may have implications beyond muscle for hereditary spherocytosis, as KCTD6 is also present in erythrocytes, and erythrocyte ankyrin isoforms contain its mapped minimal binding site