Bond Strength of Fusion Bonded Epoxy-Coated Reinforcement in Concrete

Fusion-bonded epoxy-coated steel is expected to extend the service life of the reinforced concrete structure in chloride-laden environments. However, the effect of coating on the bond-strength between rebar and concrete is not well understood yet. This research, therefore, studied the effect of epoxy-coating on the bond characteristics of reinforcing bars in concrete. The bond characteristics were assessed through pullout test considering variables viz. concrete strength, embedded length and bar diameter. The load was applied to reinforcing bars embedded in concrete until bond strength between the bar and concrete exceeded. Bond strength of epoxy-coated bars was compared with that of the uncoated bars. It was found that epoxy-coating reduced the bond strength approximately 25% for Ø20mm bar and 12% for Ø16mm and Ø12mm bar. As with uncoated bar, bond strength of coated bars were also increased with concrete strength. However, the bond strength ratio between coated and uncoated bars was found almost independent of concrete strength. Based on the test results, a development length modification factor of 1.33 is proposed for Ø20mm bar and 1.15 for Ø12mm and Ø16mm bar to compensate the bond strength reduction due to the epoxy coating

Optimal Control of Connected Automated Vehicles with Event-Triggered Control Barrier Functions: a Test Bed for Safe Optimal Merging

We address the problem of controlling Connected and Automated Vehicles (CAVs) in conflict areas of a traffic network subject to hard safety constraints. It has been shown that such problems can be solved through a combination of tractable optimal control problems and Control Barrier Functions (CBFs) that guarantee the satisfaction of all constraints. These solutions can be reduced to a sequence of Quadratic Programs (QPs) which are efficiently solved on line over discrete time steps. However, guaranteeing the feasibility of the CBF-based QP method within each discretized time interval requires the careful selection of time steps which need to be sufficiently small. This creates computational requirements and communication rates between agents which may hinder the controller's application to real CAVs. In this paper, we overcome this limitation by adopting an event-triggered approach for CAVs in a conflict area such that the next QP is triggered by properly defined events with a safety guarantee. We present a laboratory-scale test bed we have developed to emulate merging roadways using mobile robots as CAVs which can be used to demonstrate how the event-triggered scheme is computationally efficient and can handle measurement uncertainties and noise compared to time-driven control while guaranteeing safety.Comment: arXiv admin note: substantial text overlap with arXiv:2203.12089, arXiv:2209.1305

Trust-Aware Resilient Control and Coordination of Connected and Automated Vehicles

We address the security of a network of Connected and Automated Vehicles (CAVs) cooperating to navigate through a conflict area. Adversarial attacks such as Sybil attacks can cause safety violations resulting in collisions and traffic jams. In addition, uncooperative (but not necessarily adversarial) CAVs can also induce similar adversarial effects on the traffic network. We propose a decentralized resilient control and coordination scheme that mitigates the effects of adversarial attacks and uncooperative CAVs by utilizing a trust framework. Our trust-aware scheme can guarantee safe collision free coordination and mitigate traffic jams. Simulation results validate the theoretical guarantee of our proposed scheme, and demonstrate that it can effectively mitigate adversarial effects across different traffic scenarios.Comment: Keywords: Resilient control and coordination, Cybersecurity, Safety guaranteed coordination, Connected And Autonomous Vehicle

Identification and characterization of Dlc1 isoforms in the mouse and study of the biological function of a single gene trapped isoform

<p>Abstract</p> <p>Background</p> <p>The Dlc1 (deleted in liver cancer 1) tumour suppressor gene codes for a RhoGTPase activating protein that is found inactivated in many tumour types. Several transcriptional isoforms have been described but the functional significance and tissue distribution of each form is presently poorly understood. Also, differences in the number of isoforms and splice variants reported still exist between different mammalian species. In order to better understand the number and function of the different variants of the Dlc1 gene in the mouse, we have carried out a detailed analysis. Extensive 3' RACE experiments were carried out in order to identify all possible Dlc1 isoforms and splice variants in the mouse. In addition, we have generated a gene trapped mouse that targets one of these isoforms in order to study its biological function. The effect of this gene trap insertion on the splicing of other isoforms has also been studied.</p> <p>Results</p> <p>In addition to the known 6.1 and 6.2 Kb transcripts of Dlc1, our study revealed the existence of a novel 7.6 Kb transcriptional isoform in the mouse, which corresponds to the human 7.4 Kb (KIAA1723) cDNA transcript. A gene trapped embryonic cell line, with an insertion between Exon 1 and 2 of the 6.1 Kb transcriptional isoform, was used to generate a transgenic mouse. This line showed a significant reduction in the expression of the trapped isoform. However, reduced expression of the other isoforms was not seen. Mice heterozygous for the gene trapped allele were phenotypically normal, but homozygous mutant embryos did not survive beyond 10.5 days post coitum. Dlc1^gt/gtembryos showed defects in the brain, heart, and placental blood vessels. Cultured serum-free mouse embryo cells from Dlc1 deficient embryos had elevated RhoA activity and displayed alterations in the organization of actin filaments and focal adhesions. The Dlc1 deficient cells also exhibited increased wound closure in an <it>in vitro </it>scratch assay.</p> <p>Conclusions</p> <p>The mouse has three major transcriptional isoforms of the Dlc1 gene that are differentially expressed in various tissues. A mouse with exon 1 of the 6.1 Kb transcript gt resulted in hypomorphic expression of Dlc1 protein and an embryonic lethal phenotype in the homozygous condition, which indicates that this isoform plays a major role in mouse development. The Dlc1 deficient cells showed altered cytoskeleton structure, increased RhoA activity and cellular migration.</p

Pion Valence Structure from Ioffe-Time Parton Pseudodistribution Functions

We present a calculation of the pion valence quark distribution extracted using the formalism of reduced Ioffe-time pseudodistributions or more commonly known as pseudo-PDFs. Our calculation is carried out on two different 2 + 1 flavor QCD ensembles using the isotropic-clover fermion action, with lattice dimensions 243 × 64 and 323 × 96 at the lattice spacing of a = 0.127 fm, and with the quark mass equivalent to a pion mass of mπ ≃ 415 MeV. We incorporate several combinations of smeared-point and smeared-smeared pion source-sink interpolation fields in obtaining the lattice QCD matrix elements using the summation method. After one-loop perturbative matching and combining the pseudodistributions from these two ensembles, we extract the pion valence quark distribution using a phenomenological functional form motivated by the global fits of parton distribution functions. We also calculate the lowest four moments of the pion quark distribution through the “operator product expansion without operator product expansion.” We present a qualitative comparison between our lattice QCD extraction of the pion valence quark distribution with that obtained from global fits and previous lattice QCD calculations

Muscarinic Acetylcholine Type 1 Receptor Activity Constrains Neurite Outgrowth by Inhibiting Microtubule Polymerization and Mitochondrial Trafficking in Adult Sensory Neurons

The muscarinic acetylcholine type 1 receptor (M1R) is a metabotropic G protein-coupled receptor. Knockout of M1R or exposure to selective or specific receptor antagonists elevates neurite outgrowth in adult sensory neurons and is therapeutic in diverse models of peripheral neuropathy. We tested the hypothesis that endogenous M1R activation constrained neurite outgrowth via a negative impact on the cytoskeleton and subsequent mitochondrial trafficking. We overexpressed M1R in primary cultures of adult rat sensory neurons and cell lines and studied the physiological and molecular consequences related to regulation of cytoskeletal/mitochondrial dynamics and neurite outgrowth. In adult primary neurons, overexpression of M1R caused disruption of the tubulin, but not actin, cytoskeleton and significantly reduced neurite outgrowth. Over-expression of a M1R-DREADD mutant comparatively increased neurite outgrowth suggesting that acetylcholine released from cultured neurons interacts with M1R to suppress neurite outgrowth. M1R-dependent constraint on neurite outgrowth was removed by selective (pirenzepine) or specific (muscarinic toxin 7) M1R antagonists. M1R-dependent disruption of the cytoskeleton also diminished mitochondrial abundance and trafficking in distal neurites, a disorder that was also rescued by pirenzepine or muscarinic toxin 7. M1R activation modulated cytoskeletal dynamics through activation of the G protein (Gα13) that inhibited tubulin polymerization and thus reduced neurite outgrowth. Our study provides a novel mechanism of M1R control of Gα13 protein-dependent modulation of the tubulin cytoskeleton, mitochondrial trafficking and neurite outgrowth in axons of adult sensory neurons. This novel pathway could be harnessed to treat dying-back neuropathies since anti-muscarinic drugs are currently utilized for other clinical conditions