1000 resultados para Elastic Proteins


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The Series Elasic Actuator has been proposed as a method for providing safe force or torque based acutation for robots that interact with humans. In this paper we look at some outstanding issues in the implementation and control of Series Elastic Actuators. The study addresses issues in making the Series Elastic Actuator respond effectively in the presence of physical difficulties such as restriction, using a computation efficient controller. The improvement over previous implementations is achieved by treating the motor as a velocity source to the elastic element, rather than as a torque source.

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The Velocity Sourced Series Elastic Actuator has been proposed as a method for providing safe force or torque based actuation for robots without compromising the actuator performance. In this paper we assess the safety of Velocity Sourced Series Elastic Actuators by measuring the Head Injury Criterion scores for collisions with a model head. The study makes a comparative analysis against stiff, high impedance actuation using the same motor without the series elastic component, showing that the series elastic component brings about a massive reduction in the chance of head injury. The benefits of a collision detection and safe reaction system are shown to be limited to collisions at low speeds, providing greater interaction comfort but not necessarily contributing to safety from injury.

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Actuators with deliberately added compliant elements in the transmission system are often described as improving the safety of the actuator at the detriment of the performance. We show that our variant of the Series Elastic Actuator topology, the Velocity Sourced Series Elastic Actuator, has well defined performance characteristics that make for improvements in safety and performance over conventional high impedance actuators. The improvement in performance was principally achieved by having tight velocity control of the DC motor that acts as the mechanical power source for the actuator. Results for performance are given for point to point transition times, while results for safety are based on empirical assessment of the Head Injury Criterion during collisions.

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LiteSteel beam (LSB) is a new cold-formed steel hollow flange channel beam. The unique LSB section is produced by a patented manufacturing process involving simultaneous cold-forming and dual electric resistance welding. To date, limited research has been undertaken on the shear buckling behaviour of LSBs with torsionally rigid, rectangular hollow flanges. For the shear design of LSB web panels, their elastic shear buckling strength must be determined accurately including the potential post-buckling strength. Currently the elastic shear buckling coefficients of web panels are determined by assuming conservatively that the web panels are simply supported at the junction between the flange and web elements. Therefore finite element analyses were carried out to investigate the elastic shear buckling behaviour of LSB sections including the effect of true support conditions at the junction between their flange and web elements. An improved equation for the higher elastic shear buckling coefficient of LSBs was developed and included in the shear capacity equations of Australian cold-formed steel codes. Predicted ultimate shear capacity results were compared with available experimental results, both of which showed considerable improvement to the shear capacities of LSBs. A study on the shear flow distribution of LSBs was also undertaken prior to the elastic buckling analysis study. This paper presents the details of this investigation and the results including the shear flow distribution of LSBs. Keywords: LiteSteel beam, Elastic shear buckling, Shear flow, Cold-formed steel structures, Slender web, Hollow flanges.

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Damage to genetic material represents a persistent and ubiquitous threat to genomic stability. Once DNA damage is detected, a multifaceted signaling network is activated that halts the cell cycle, initiates repair, and in some instances induces apoptotic cell death. In this article, we will review DNA damage surveillance networks, which maintain the stability of our genome, and discuss the efforts underway to identify chemotherapeutic compounds targeting the core components of DNA double-strand breaks (DSB) response pathway. The majority of tumor cells have defects in maintaining genomic stability owing to the loss of an appropriate response to DNA damage. New anticancer agents are exploiting this vulnerability of cancer cells to enhance therapeutic indexes, with limited normal tissue toxicity. Recently inhibitors of the checkpoint kinases Chk1 and Chk2 have been shown to sensitize tumor cells to DNA damaging agents. In addition, the treatment of BRCA1- or BRCA2-deficient tumor cells with poly(ADP-ribose) polymerase (PARP) inhibitors also leads to specific tumor killing. Due to the numerous roles of p53 in genomic stability and its defects in many human cancers, therapeutic agents that restore p53 activity in tumors are the subject of multiple clinical trials. In this article we highlight the proteins mentioned above and catalog several additional players in the DNA damage response pathway, including ATM, DNA-PK, and the MRN complex, which might be amenable to pharmacological interventions and lead to new approaches to sensitize cancer cells to radio- and chemotherapy. The challenge is how to identify those patients most receptive to these treatments.

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DNA exists predominantly in a duplex form that is preserved via specific base pairing. This base pairing affords a considerable degree of protection against chemical or physical damage and preserves coding potential. However, there are many situations, e.g. during DNA damage and programmed cellular processes such as DNA replication and transcription, in which the DNA duplex is separated into two singlestranded DNA (ssDNA) strands. This ssDNA is vulnerable to attack by nucleases, binding by inappropriate proteins and chemical attack. It is very important to control the generation of ssDNA and protect it when it forms, and for this reason all cellular organisms and many viruses encode a ssDNA binding protein (SSB). All known SSBs use an oligosaccharide/oligonucleotide binding (OB)-fold domain for DNA binding. SSBs have multiple roles in binding and sequestering ssDNA, detecting DNA damage, stimulating strand-exchange proteins and helicases, and mediation of protein–protein interactions. Recently two additional human SSBs have been identified that are more closely related to bacterial and archaeal SSBs. Prior to this it was believed that replication protein A, RPA, was the only human equivalent of bacterial SSB. RPA is thought to be required for most aspects of DNA metabolism including DNA replication, recombination and repair. This review will discuss in further detail the biological pathways in which human SSBs function.

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Hydrogels, which are three-dimensional crosslinked hydrophilic polymers, have been used and studied widely as vehicles for drug delivery due to their good biocompatibility. Traditional methods to load therapeutic proteins into hydrogels have some disadvantages. Biological activity of drugs or proteins can be compromised during polymerization process or the process of loading protein can be really timeconsuming. Therefore, different loading methods have been investigated. Based on the theory of electrophoresis, an electrochemical gradient can be used to transport proteins into hydrogels. Therefore, an electrophoretic method was used to load protein in this study. Chemically and radiation crosslinked polyacrylamide was used to set up the model to load protein electrophoretically into hydrogels. Different methods to prepare the polymers have been studied and have shown the effect of the crosslinker (bisacrylamide) concentration on the protein loading and release behaviour. The mechanism of protein release from the hydrogels was anomalous diffusion (i.e. the process was non-Fickian). The UV-Vis spectra of proteins before and after reduction show that the bioactivities of proteins after release from hydrogel were maintained. Due to the concern of cytotoxicity of residual monomer in polyacrylamide, poly(2-hydroxyethyl- methacrylate) (pHEMA) was used as the second tested material. In order to control the pore size, a polyethylene glycol (PEG) porogen was introduced to the pHEMA. The hydrogel disintegrated after immersion in water indicating that the swelling forces exceeded the strength of the material. In order to understand the cause of the disintegration, several different conditions of crosslinker concentration and preparation method were studied. However, the disintegration of the hydrogel still occurred after immersion in water principally due to osmotic forces. A hydrogel suitable for drug delivery needs to be biocompatible and also robust. Therefore, an approach to improving the mechanical properties of the porogen-containing pHEMA hydrogel by introduction of an inter-penetrating network (IPN) into the hydrogel system has been researched. A double network was formed by the introduction of further HEMA solution into the system by both electrophoresis and slow diffusion. Raman spectroscopy was used to observe the diffusion of HEMA into the hydrogel prior to further crosslinking by ã-irradiation. The protein loading and release behaviour from the hydrogel showing enhanced mechanical property was also studied. Biocompatibility is a very important factor for the biomedical application of hydrogels. Different hydrogels have been studied on both a three-dimensional HSE model and a HSE wound model for their biocompatibilities. They did not show any detrimental effect to the keratinocyte cells. From the results reported above, these hydrogels show good biocompatibility in both models. Due to the advantage of the hydrogels such as the ability to absorb and deliver protein or drugs, they have potential to be used as topical materials for wound healing or other biomedical applications.

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The elastic task model, a significant development in scheduling of real-time control tasks, provides a mechanism for flexible workload management in uncertain environments. It tells how to adjust the control periods to fulfill the workload constraints. However, it is not directly linked to the quality-of-control (QoC) management, the ultimate goal of a control system. As a result, it does not tell how to make the best use of the system resources to maximize the QoC improvement. To fill in this gap, a new feedback scheduling framework, which we refer to as QoC elastic scheduling, is developed in this paper for real-time process control systems. It addresses the QoC directly through embedding both the QoC management and workload adaptation into a constrained optimization problem. The resulting solution for period adjustment is in a closed-form expressed in QoC measurements, enabling closed-loop feedback of the QoC to the task scheduler. Whenever the QoC elastic scheduler is activated, it improves the QoC the most while still meeting the system constraints. Examples are given to demonstrate the effectiveness of the QoC elastic scheduling.