Robust Control of Robotic Manipulators in the Task-Space Using an Adaptive Observer Based on Chebyshev Polynomials

In this paper, an adaptive observer for robust control of robotic manipulators is proposed.The lumped uncertainty is estimated using Chebyshev polynomials. Usually, the uncertainty upper bound is required in designing observer-controller structures. However, obtaining this bound is a challenging task. To solve this problem, many uncertainty estimation techniques have been proposed in the literature based on neuro-fuzzy systems. As an alternative, in this paper, Chebyshev polynomials have been applied to uncertainty estimation due to their simpler structure and less computational load.Based on strictly-positive-real(SPR) Lyapunov theory, the stability of the closed-loop system can be verified. The Chebyshev coefficients are tuned based on the adaptation rules obtained in the stability analysis. Also, to compensate the truncation error of the Chebyshev polynomials, a continuous robust control term is designed while in previous related works, usually a discontinuous term is used. An SCARA manipulator actuated by permanent magnet DC motors is used for computer simulations.Simulation results reveal the superiority of the designed method.     

Evolution and biology of supernumerary B chromosomes

B chromosomes (Bs) are dispensable components of the genome exhibiting non-Mendelian inheritance and have been widely reported on over several thousand eukaryotes, but still remain an evolutionary mystery ever since their first discovery over a century ago [1]. Recent advances in genome analysis have significantly improved our knowledge on the origin and composition of Bs in the last few years. In contrast to the prevalent view that Bs do not harbor genes, recent analysis revealed that Bs of sequenced species are rich in gene-derived sequences. We summarize the latest findings on supernumerary chromosomes with a special focus on the origin, DNA composition, and the non-Mendelian accumulation mechanism of Bs.     

The common fragile site FRA16D gene product WWOX: roles in tumor suppression and genomic stability

The fragile WWOX gene, encompassing the chromosomal fragile site FRA16D, is frequently altered in human cancers. While vulnerable to DNA damage itself, recent evidence has shown that the WWOX protein is essential for proper DNA damage response (DDR). Furthermore, the gene product, WWOX, has been associated with multiple protein networks, highlighting its critical functions in normal cell homeostasis. Targeted deletion of Wwox in murine models suggests its in vivo requirement for proper growth, metabolism, and survival. Recent molecular and biochemical analyses of WWOX functions highlighted its role in modulating aerobic glycolysis and genomic stability. Cumulatively, we propose that the gene product of FRA16D, WWOX, is a functionally essential protein that is required for cell homeostasis and that its deletion has important consequences that contribute to the neoplastic process. This review discusses the essential role of WWOX in tumor suppression and genomic stability and how its alteration contributes to cancer transformation.     

Mineralogical and sink-float studies of Jajarm low-grade bauxite

Jajarm’s bauxite deposits are mainly diasporic, and they have a low mass ratio of Al₂O₃/SiO₂. It is necessary to increase the run-of-mine mass ratio before feeding the material to the Bayer process. Chemical analysis indicated that the low-grade bauxite sample from Jajarm contained 43.9wt% Al₂O₃ and 13.35wt% SiO₂, resulting in a mass ratio of 3.29. According to mineralogical studies, the presence of aluminosilicate minerals such as kaolinite, illite, and quartz was the main reason for the decrease of the mass ratio. Microscopic observations revealed that, with the size reduction from -1000+710 to -38 μm, the liberation degree of diaspore increased from 10% to 60%, and that of aluminosilicates increased from 20% to 85%. Heavy liquids with the densities of 2.8, 3.0, 3.2, and 3.4 g/cm3 were used to evaluate the heavy media separation in three sizes, i.e., -3350+710, -710+212, and -212+125 μm. Laboratory studies confirm that the density of 3.2 g/cm3 can produce the concentrates (in sunk fractions) with recoveries of 89.09%, 91.24%, and 84.68% with the Al₂O₃/SiO₂ mass ratios of 5.03, 5.16, and 5.15 for the -3350+710, -710+212, and -212+125 μm sizes, respectively.     

tRNA splicing endonuclease mutations cause pontocerebellar hypoplasia

Pontocerebellar hypoplasias (PCH) represent a group of neurodegenerative autosomal recessive disorders with prenatal onset, atrophy or hypoplasia of the cerebellum, hypoplasia of the ventral pons, microcephaly, variable neocortical atrophy and severe mental and motor impairments. In two subtypes, PCH2 and PCH4, we identified mutations in three of the four different subunits of the tRNA-splicing endonuclease complex. Our findings point to RNA processing as a new basic cellular impairment in neurological disorders.     

CT Brain Image: Abnormalities Recognition and Segmentation

In order to develop an automated segmentation system for Computed Tomography (CT) brain images, a new approach which consists of several unsupervised segmentation techniques was introduced. The system segments the CT brain images into three partitions, i. e., abnormalities, cerebrospinal fluid (CSF), and brain matter. Our approach consists of two phase-segmentation methods. In the first phase segmentation, k-means and fuzzy c-means (FCM) methods were implemented to segment and transform the images into the binary images. Based on the connected component in binary images, a decision tree was employed for the annotation of normal or abnormal regions, In the second phase segmentation, the modified FCM with population-diameter independent (PDI) segmentation was applied to segment the images into CSF and brain matter. The experimental results have shown that our proposed system is feasible and yield satisfactory results.     

RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)

Activated RAS promotes dimerization of members of the RAF kinase family. ATP-competitive RAF inhibitors activate ERK signalling by transactivating RAF dimers. In melanomas with mutant BRAF(V600E), levels of RAS activation are low and these drugs bind to BRAF(V600E) monomers and inhibit their activity. This tumour-specific inhibition of ERK signalling results in a broad therapeutic index and RAF inhibitors have remarkable clinical activity in patients with melanomas that harbour mutant BRAF(V600E). However, resistance invariably develops. Here, we identify a new resistance mechanism. We find that a subset of cells resistant to vemurafenib (PLX4032, RG7204) express a 61-kDa variant form of BRAF(V600E), p61BRAF(V600E), which lacks exons 4-8, a region that encompasses the RAS-binding domain. p61BRAF(V600E) shows enhanced dimerization in cells with low levels of RAS activation, as compared to full-length BRAF(V600E). In cells in which p61BRAF(V600E) is expressed endogenously or ectopically, ERK signalling is resistant to the RAF inhibitor. Moreover, a mutation that abolishes the dimerization of p61BRAF(V600E) restores its sensitivity to vemurafenib. Finally, we identified BRAF(V600E) splicing variants lacking the RAS-binding domain in the tumours of six of nineteen patients with acquired resistance to vemurafenib. These data support the model that inhibition of ERK signalling by RAF inhibitors is dependent on levels of RAS-GTP too low to support RAF dimerization and identify a novel mechanism of acquired resistance in patients: expression of splicing isoforms of BRAF(V600E) that dimerize in a RAS-independent manner.     

Bandwidth optimization of a Planar Inverted-F Antenna using binary and real coded genetic algorithms

With the exponential development of mobile communications and the miniaturization of radio frequency transceivers, the need for small and low profile antennas at mobile frequencies is constantly growing. Therefore, new antennas should be developed to provide larger bandwidth and at the same time small dimensions. Although the gain in bandwidth performances of an antenna are directly related to its dimensions in relation to the wavelength, the aim is to keep the overall size of the antenna constant and from there, find the geometry and structure that give the best performance. The design and bandwidth optimization of a Planar Inverted-F Antenna (PIFA) were introduced in order to achieve a larger bandwidth in the 2 GHz band, using two optimization techniques based upon genetic algorithms (GA), namely the Binary Coded GA (BCGA) and Real-Coded GA (RCGA). During the optimization process, the different PIFA models were evaluated using the finite-difference time domain (FDTD) method-a technique belonging to the general class of differential time domain numerical modeling methods.