Templates and anchors for antenna-based wall following in cockroaches and robots

The interplay between robotics and neuromechanics facilitates discoveries in both fields: nature provides roboticists with design ideas, while robotics research elucidates critical features that confer performance advantages to biological systems. Here, we explore a system particularly well suited to exploit the synergies between biology and robotics: high-speed antenna-based wall following of the American cockroach (Periplaneta americana). Our approach integrates mathematical and hardware modeling with behavioral and neurophysiological experiments. Specifically, we corroborate a prediction from a previously reported wall-following template - the simplest model that captures a behavior - that a cockroach antenna-based controller requires the rate of approach to a wall in addition to distance, e.g., in the form of a proportional-derivative (PD) controller. Neurophysiological experiments reveal that important features of the wall-following controller emerge at the earliest stages of sensory processing, namely in the antennal nerve. Furthermore, we embed the template in a robotic platform outfitted with a bio-inspired antenna. Using this system, we successfully test specific PD gains (up to a scale) fitted to the cockroach behavioral data in a "real-world" setting, lending further credence to the surprisingly simple notion that a cockroach might implement a PD controller for wall following. Finally, we embed the template in a simulated lateral-leg-spring (LLS) model using the center of pressure as the control input. Importantly, the same PD gains fitted to cockroach behavior also stabilize wall following for the LLS model. © 2008 IEEE.

Anchors, scales and the relative coding of value in the brain.

People are alarmingly susceptible to manipulations that change both their expectations and experience of the value of goods. Recent studies in behavioral economics suggest such variability reflects more than mere caprice. People commonly judge options and prices in relative terms, rather than absolutely, and display strong sensitivity to exemplar and price anchors. We propose that these findings elucidate important principles about reward processing in the brain. In particular, relative valuation may be a natural consequence of adaptive coding of neuronal firing to optimise sensitivity across large ranges of value. Furthermore, the initial apparent arbitrariness of value may reflect the brains' attempts to optimally integrate diverse sources of value-relevant information in the face of perceived uncertainty. Recent findings in neuroscience support both accounts, and implicate regions in the orbitofrontal cortex, striatum, and ventromedial prefrontal cortex in the construction of value.

Plastic limit solution for the response of plate anchors under combined translational and torsional undrained loading

Plate anchors are increasingly being used to moor large floating offshore structures in deep and ultradeep water. These facilities impart substantial vertical uplift loading to plate anchors. However, extreme operating conditions such as hurricane loading often result in partial system failures, with significant change in the orientation of the remaining intact mooring lines. The purpose of this study is to investigate the undrained pure translational (parallel to plate) and torsional bearing capacity of anchor plates idealized as square and rectangular shaped plates. Moreover, the interaction response of plate anchors under combined translational and torsional loading is studied using a modified plastic limit analysis (PLA) approach. The previous PLA formulation which did not account for shear-normal force interaction on the vertical end faces of the plate provides an exact solution to the idealized problem of an infinitely thin plate but only an approximate solution to the problem of a plate of finite thickness. This is also confirmed by the three-dimensional finite element (FE) results, since the PLA values exceed FE results as the thickness of the plate increases. By incorporating the shear-normal interaction relationship in the modified solution, the torsional bearing capacity factors, as well as the plate interaction responses are enhanced as they show satisfactory agreement with the FE results. The interaction relationship is then obtained for square and rectangular plates of different aspect ratios and thicknesses. The new interaction relationships could also be used as an associated plastic failure locus for combined shear and torsional loading to predict plastic displacements and rotations in translational and torsional loading modes as well. Copyright © 2011 by the International Society of Offshore and Polar Engineers (ISOPE).

Analysis and comparison of displacement granular pile anchors

Granular piles can resist only compressive and shear loads owing to their inherent nature. By a simple modification of providing a pedestal/geogrid at the bottom and attaching a cable to the same, they are made to resist pullout/uplift forces. This paper presents an analysis of granular pile anchor (GPA), considering it and the in situ soil to behave linearly and the in situ ground to be semi-infinite. A parametric study presents results in the form of variations of normalised shear stress, displacement influence coefficient and axial uplift force with depth with relative stiffness factor. Two methods for the estimation of deformation moduli of the GPA and the in situ soil are proposed. Based on the estimated values of the moduli, the displacements of GPA were estimated and the results compared with test results of Kumar (2002). The predicted displacements compare well with the measured ones.

Granular anchors under vertical loading - axial pull

Granular anchors are a relatively new concept in ground engineering with relatively little known regarding their load–displacement behaviour, failure modes, ultimate pullout capacity and also potential applications. A granular anchor consists of three main components: a base plate; tendon and compacted granular backfill. The tendon is used to transmit the applied load to the base plate which compresses the granular material to form the anchor. A study of the load–displacement response and ultimate pullout capacity of granular anchors constructed in intact lodgement till and made ground deposits is reported in this paper. Parallel tests were also performed on cast insitu concrete anchors which are traditionally used for anchoring purposes. A new method of analysis for the determination of the ultimate pullout capacity of granular anchors is presented and verified experimentally, with the dominant mode of failure controlled by the column length to diameter ratio. Granular anchors with L/D > 7 principally failed on bulging whereas short granular anchors failed on shaft resistance, with the latter mobilising similar pullout capacities as conventional concrete anchors.

Transcriptional regulation of the mannosyltransferase-encoding gene pigm in inherited glycosylphosphatidylinositol (GPI) deficiency

RESUMO:O glicosilfosfatidilinositol (GPI) é um complexo glicolipídico utlizado por dezenas de proteínas, o qual medeia a sua ancoragem à superfície da célula. Proteínas de superfície celular ancoradas a GPI apresentam várias funções essenciais para a manutenção celular. A deficiência na síntese de GPI é o que caracteriza principalmente a deficiência hereditária em GPI, um grupo de doenças autossómicas raras que resultam de mutações nos genes PIGA, PIGL, PIGM, PIGV, PIGN, PIGO e PIGT, os quais sao indispensáveis para a biossíntese do GPI. Uma mutação pontual no motivo rico em GC -270 no promotor de PIGM impede a ligação do factor de transcrição (FT) Sp1 à sua sequência de reconhecimento, impondo a compactação da cromatina, associada à hipoacetilação de histonas, e consequentemente, impedindo a transcrição de PIGM. Desta forma, a adição da primeira manose ao GPI é comprometida, a síntese de GPI diminui assim como as proteínas ligadas a GPI à superficie das células. Pacientes com Deficiência Hereditária em GPI-associada a PIGM apresentam trombose e epilesia, e ausência de hemólise intravascular e anemia, sendo que estas duas últimas características definem a Hemoglobinúria Paroxística Nocturna (HPN), uma doença rara causada por mutações no gene PIGA. Embora a mutação que causa IGD seja constitutiva e esteja presente em todos os tecidos, o grau de deficiência em GPI varia entre células do mesmo tecido e entre células de tecidos diferentes. Por exemplo nos granulócitos e linfócitos B a deficiência em GPI é muito acentuada mas nos linfócitos T, fibroblastos, plaquetas e eritrócitos é aproximadamente normal, daí a ausência de hemólise intravascular. Os eventos transcricionais que estão na base da expressão diferencial da âncora GPI nas células hematopoiéticas são desconhecidos e constituem o objectivo geral desta tese. Em primeiro lugar, os resultados demonstraram que os níveis de PIGM mRNA variam entre células primárias hematopoiéticas normais. Adicionalmente, a configuração dos nucleossomas no promotor de PIGM é mais compacta em células B do que em células eritróides e tal está correlacionado com os níveis de expressão de PIGM, isto é, inferior nas células B. A presença de vários motivos de ligação para o FT específico da linhagem megacariocítica-eritróide GATA-1 no promotor de PIGM sugeriu que GATA-1 desempenha um papel regulador na sua transcrição. Os resultados mostraram que muito possivelmente GATA-1 desempenha um papel repressor em vez de activador da expressão de PIGM. Resultados preliminares sugerem que KLF1, um factor de transcrição restritamente eritróide, regula a transcrição de PIGM independentemente do motivo -270GC. Em segundo lugar, a investigação do papel dos FTs Sp demonstrou que Sp1 medeia directamente a transcrição de PIGM em ambas as células B e eritróide. Curiosamente, ao contrário do que acontece nas células B, em que a transcrição de PIGM requer a ligação do FT geral Sp1 ao motivo -270GC, nas células eritróides Sp1 regula a transcrição de PIGM ao ligar-se a montante e não ao motivo -270GC. Para além disso, demonstrou-se que Sp2 não é um regulador directo da transcrição de PIGM quer nas células B quer nas células eritróides. Estes resultados explicam a ausência de hemólise intravascular nos doentes com IGD associada a PIGM, uma das principais características que define a HPN. Por último, resultados preliminares mostraram que a repressão da transcrição de PIGM devida à mutação patogénica -270C>G está associada com a diminuição da frequência de interacções genómicas em cis entre PIGM e os seus genes “vizinhos”, sugerindo adicionalmente que a regulação de PIGM e desses genes é partilhada. No seu conjunto, os resultados apresentados nesta tese contribuem para o conhecimento do controlo transcricional de um gene housekeeping, específico-detecido, por meio de FTs genéricos e específicos de linhagem.-------------ABSTRACTC: Glycosylphosphatidylinositol (GPI) is a complex glycolipid used by dozens of proteins for cell surface anchoring. GPI-anchored proteins have various functions that are essential for the cellular maintenance. Defective GPI biosynthesis is the hallmark of inherited GPI deficiency (IGD), a group of rare autosomal diseases caused by mutations in PIGA, PIGL, PIGM, PIGV, PIGN, PIGO and PIGT, all genes indispensable for GPI biosynthesis. A point mutation in the -270GC-rich box in the core promoter of PIGM disrupts binding of the transcription factor (TF) Sp1 to it, imposing nucleosome compaction associated with histone hypoacetylation, thus abrogating transcription of PIGM. As a consequence of PIGM transcriptional repression, addition of the first mannose residue onto the GPI core and thus GPI production are impaired; and expression of GPI-anchored proteins on the surface of cells is severely impaired. Patients with PIGM-associated IGD suffer from life-threatening thrombosis and epilepsy but not intravascular haemolysis and anaemia, two defining features of paroxysmal nocturnal haemoglobinuria (PNH), a rare disease caused by somatic mutations in PIGA. Although the disease-causing mutation in IGD is constitutional and present in all tissues, the degree of GPI deficiency is variable and differs between cells of the same and of different tissues. Accordingly, GPI deficiency is severe in granulocytes and B cells but mild in T cells, fibroblasts, platelets and erythrocytes, hence the lack of intravascular haemolysis.The transcriptional events underlying differential expression of GPI in the haematopoietic cells of PIG-M-associated IGD are not known and constitute the general aim of this thesis. Firstly, I found that PIGM mRNA levels are variable amongst normal primary haematopoietic cells. In addition, the nucleosome configuration in the promoter of PIGM is more compacted in B cells than in erythroid cells and this correlated with the levels of PIGM mRNA expression, i.e., lower in B cells. The presence of several binding sites for GATA-1, a mega-erythroid lineage-specific transcription factor (TF), at the PIGM promoter suggested that GATA-1 has a role on PIGM transcription. My results showed that GATA-1 in erythroid cells is most likely a repressor rather than an activator of PIGM expression. Preliminary data suggested that KLF1, an erythroid-specific TF, regulates PIGM transcription but independently of the -270GC motif. Secondly, investigation of the role of the Sp TFs showed that Sp1 directly mediates PIGM transcriptional regulation in both B and erythroid cells. However, unlike in B cells in which active PIGM transcription requires binding of the generic TF Sp1 to the -270GC-rich box, in erythroid cells, Sp1 regulates PIGM transcription by binding upstream of but not to the -270GC-rich motif. Additionally, I showed that Sp2 is not a direct regulator of PIGM transcription in B and erythroid cells. These findings explain lack of intravascular haemolysis in PIGM-associated IGD, a defining feature of PNH. Lastly, preliminary work shows that transcriptional repression of PIG-M by the pathogenic -270C>G mutation is associated with reduced frequency of in cis genomic interactions between PIGM and its neighbouring genes, suggesting a shared regulatory link between these genes and PIGM. Altogether, the results presented in this thesis provide novel insights into tissuespecific transcriptional control of a housekeeping gene by lineage-specific and generic TFs.

Borg's rating of perceived exertion scales: do the verbal anchors mean the same for different clinical groups?

Objective: To examine the interpretation of the verbal anchors used in the Borg rating of perceived exertion (RPE) scales in different clinical groups and a healthy control group. Design: Prospective experimental study. Setting: Rehabilitation center. Participants: Nineteen subjects with brain injury, 16 with chronic low back pain (CLBP), and 20 healthy controls. Interventions: Not applicable. Main Outcome Measures: Subjects used a visual analog scale (VAS) to rate their interpretation of the verbal anchors from the Borg RPE 6-20 and the newer 10-point category ratio scale. Results: All groups placed the verbal anchors in the order that they occur on the scales. There were significant within-group differences (P > .05) between VAS scores for 4 verbal anchors in the control group, 8 in the CLBP group, and 2 in the brain injury group. There was no significant difference in rating of each verbal anchor between the groups (P > .05). Conclusions: All subjects rated the verbal anchors in the order they occur on the scales, but there was less agreement in rating of each verbal anchor among subjects in the brain injury group. Clinicians should consider the possibility of small discrepancies in the meaning of the verbal anchors to subjects, particularly those recovering from brain injury, when they evaluate exercise perceptions.

Nominal anchors and macroeconomic coordination options in MERCOSUR

Includes bibliography

Application of Submerged Grouted Anchors in Sheet Pile Quay Walls

Sheet pile walls are one of the oldest earth retention systems utilized in civil engineering projects. They are used for various purposes; such as excavation support system, cofferdams, cut-off walls under dams, slope stabilization, waterfront structures, and flood walls. Sheet pile walls are one of the most common types of quay walls used in port construction. The worldwide increases in utilization of large ships for transportation have created an urgent need of deepening the seabed within port areas and consequently the rehabilitation of its wharfs. Several methods can be used to increase the load-carrying capacity of sheet-piling walls. The use of additional anchored tie rods grouted into the backfill soil and arranged along the exposed wall height is one of the most practical and appropriate solutions adopted for stabilization and rehabilitation of the existing quay wall. The Ravenna Port Authority initiated a project to deepen the harbor bottom at selected wharves. An extensive parametric study through the finite element program, PLAXIS 2D, version 2012 was carried out to investigate the enhancement of using submerged grouted anchors technique on the load response of sheet-piling quay wall. The influence of grout-ties area, length of grouted body, anchor inclination and anchor location were considered and evaluated due to the effect of different system parameters. Also a comparative study was conducted by Plaxis 2D and 3D program to investigate the behavior of these sheet pile quay walls in terms of horizontal displacements induced along the sheet pile wall and ground surface settlements as well as the anchor force and calculated factor of safety. Finally, a comprehensive study was carried out by using different constitutive models to simulate the mechanical behavior of the soil to investigate the effect of these two models (Mohr-Coulomb and Hardening Soil) on the behavior of these sheet pile quay walls.

myo-Inositol uptake is essential for bulk inositol phospholipid but not glycosylphosphatidylinositol synthesis in Trypanosoma brucei

myo-Inositol is an essential precursor for the production of inositol phosphates and inositol phospholipids in all eukaryotes. Intracellular myo-inositol is generated by de novo synthesis from glucose 6-phosphate or is provided from the environment via myo-inositol symporters. We show that in Trypanosoma brucei, the causative pathogen of human African sleeping sickness and nagana in domestic animals, myo-inositol is taken up via a specific proton-coupled electrogenic symport and that this transport is essential for parasite survival in culture. Down-regulation of the myo-inositol transporter using RNA interference inhibited uptake of myo-inositol and blocked the synthesis of the myo-inositol-containing phospholipids, phosphatidylinositol and inositol phosphorylceramide; in contrast, it had no effect on glycosylphosphatidylinositol production. This together with the unexpected localization of the myo-inositol transporter in both the plasma membrane and the Golgi demonstrate that metabolism of endogenous and exogenous myo-inositol in T. brucei is strictly segregated.

The Gup1 homologue of Trypanosoma brucei is a GPI glycosylphosphatidylinositol remodelase

Glycosylphosphatidylinositol (GPI) lipids of Trypanosoma brucei undergo lipid remodelling, whereby longer fatty acids on the glycerol are replaced by myristate (C14:0). A similar process occurs on GPI proteins of Saccharomyces cerevisiae where Per1p first deacylates, Gup1p subsequently reacylates the anchor lipid, thus replacing a shorter fatty acid by C26:0. Heterologous expression of the GUP1 homologue of T. brucei in gup1Delta yeast cells partially normalizes the gup1Delta phenotype and restores the transfer of labelled fatty acids from Coenzyme A to lyso-GPI proteins in a newly developed microsomal assay. In this assay, the Gup1p from T. brucei (tbGup1p) strongly prefers C14:0 and C12:0 over C16:0 and C18:0, whereas yeast Gup1p strongly prefers C16:0 and C18:0. This acyl specificity of tbGup1p closely matches the reported specificity of the reacylation of free lyso-GPI lipids in microsomes of T. brucei. Depletion of tbGup1p in trypanosomes by RNAi drastically reduces the rate of myristate incorporation into the sn-2 position of lyso-GPI lipids. Thus, tbGup1p is involved in the addition of myristate to sn-2 during GPI remodelling in T. brucei and can account for the fatty acid specificity of this process. tbGup1p can act on GPI proteins as well as on GPI lipids.

Resistance to apoptosis caused by PIG-A gene mutations in paroxysmal nocturnal hemoglobinuria

Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell disorder resulting from mutations in an X-linked gene, PIG-A, that encodes an enzyme required for the first step in the biosynthesis of glycosylphosphatidylinositol (GPI) anchors. PIG-A mutations result in absent or decreased cell surface expression of all GPI-anchored proteins. Although many of the clinical manifestations (e.g., hemolytic anemia) of the disease can be explained by a deficiency of GPI-anchored complement regulatory proteins such as CD59 and CD55, it is unclear why the PNH clone dominates hematopoiesis and why it is prone to evolve into acute leukemia. We found that PIG-A mutations confer a survival advantage by making cells relatively resistant to apoptotic death. When placed in serum-free medium, granulocytes and affected CD34+ (CD59−) cells from PNH patients survived longer than their normal counterparts. PNH cells were also relatively resistant to apoptosis induced by ionizing irradiation. Replacement of the normal PIG-A gene in PNH cell lines reversed the cellular resistance to apoptosis. Inhibited apoptosis resulting from PIG-A mutations appears to be the principle mechanism by which PNH cells maintain a growth advantage over normal progenitors and could play a role in the propensity of this disease to transform into more aggressive hematologic disorders. These data also suggest that GPI anchors are important in regulating apoptosis.

Structure of the glycosylphosphatidylinositol anchor of an arabinogalactan protein from Pyrus communis suspension-cultured cells

Arabinogalactan proteins (AGPs) are proteoglycans of higher plants, which are implicated in growth and development. We recently have shown that two AGPs, NaAGP1 (from Nicotiana alata styles) and PcAGP1 (from Pyrus communis cell suspension culture), are modified by the addition of a glycosylphosphatidylinositol (GPI) anchor. However, paradoxically, both AGPs were buffer soluble rather than membrane associated. We now show that pear suspension cultured cells also contain membrane-bound GPI-anchored AGPs. This GPI anchor has the minimal core oligosaccharide structure, d-Manα(1–2)-d-Manα(1–6)-d-Manα(1–4)-d-GlcN-inositol, which is consistent with those found in animals, protozoa, and yeast, but with a partial β(1–4)-galactosyl substitution of the 6-linked Man residue, and has a phosphoceramide lipid composed primarily of phytosphingosine and tetracosanoic acid. The secreted form of PcAGP1 contains a truncated GPI lacking the phosphoceramide moiety, suggesting that it is released from the membrane by the action of a phospholipase D. The implications of these findings are discussed in relation to the potential mechanisms by which GPI-anchored AGPs may be involved in signal transduction pathways.

The affected gene underlying the class K glycosylphosphatidylinositol (GPI) surface protein defect codes for the GPI transamidase

The final step in glycosylphosphatidylinositol (GPI) anchoring of cell surface proteins consists of a transamidation reaction in which preassembled GPI donors are substituted for C-terminal signal sequences in nascent polypeptides. In previous studies we described a human K562 cell mutant, termed class K, that accumulates fully assembled GPI units but is unable to transfer them to N-terminally processed proproteins. In further work we showed that, unlike wild-type microsomes, microsomes from these cells are unable to support C-terminal interaction of proproteins with the small nucleophiles hydrazine or hydroxylamine, and that the cells thus are defective in transamidation. In this study, using a modified recombinant vaccinia transient transfection system in conjunction with a composite cDNA prepared by 5′ extension of an existing GenBank sequence, we found that the genetic element affected in these cells corresponds to the human homolog of yGPI8, a gene affected in a yeast mutant strain exhibiting similar accumulation of GPI donors without transfer. hGPI8 gives rise to mRNAs of 1.6 and 1.9 kb, both encoding a protein of 395 amino acids that varies in cells with their ability to couple GPIs to proteins. The gene spans ≈25 kb of DNA on chromosome 1. Reconstitution of class K cells with hGPI8 abolishes their accumulation of GPI precursors and restores C-terminal processing of GPI-anchored proteins. Also, hGPI8 restores the ability of microsomes from the mutant cells to yield an active carbonyl in the presence of a proprotein which is considered to be an intermediate in catalysis by a transamidase.