Iterative Machine Learning for Precision Trajectory Tracking with Series Elastic Actuators

When robots operate in unknown environments small errors in postions can lead to large variations in the contact forces, especially with typical high-impedance designs. This can potentially damage the surroundings and/or the robot. Series elastic actuators (SEAs) are a popular way to reduce the output impedance of a robotic arm to improve control authority over the force exerted on the environment. However this increased control over forces with lower impedance comes at the cost of lower positioning precision and bandwidth. This article examines the use of an iteratively-learned feedforward command to improve position tracking when using SEAs. Over each iteration, the output responses of the system to the quantized inputs are used to estimate a linearized local system models. These estimated models are obtained using a complex-valued Gaussian Process Regression (cGPR) technique and then, used to generate a new feedforward input command based on the previous iteration's error. This article illustrates this iterative machine learning (IML) technique for a two degree of freedom (2-DOF) robotic arm, and demonstrates successful convergence of the IML approach to reduce the tracking error.Comment: 9 pages, 16 figure. Submitted to AMC Worksho

Individually-controllable magnetic artificial cilia for microfluidic manipulation tasks

Thesis (Ph.D.)--University of Washington, 2017-06This thesis presents the design, modeling, and control of a magnetic artificial cilia system in which the cilia are individually controllable. In nature, cilia exhibit metachronal waves, or a phase difference between adjacent cilia that results in a traveling wave, which may improve pumping performance or efficiency of biological cilia. However, existing magnetic artificial cilia devices typically use actuation by a rotating field generated by Helmholtz coils or by a rotating permanent magnet. These field sources cannot apply a phase shift to the cilia array and therefore cannot generate a metachronal wave. Nevertheless, magnetic actuation remains desirable for cilia devices as it allows for biocompatibility, precise control of sys- tem inputs, and low-cost fabrication of the cilia. In this thesis, a new design for magnetic artificial cilia is presented in which the actuating magnetic field is localized, enabling indi- vidual actuation. However, this design decision leads to challenging research problems in input-pattern identification, nonlinear systems modeling, and control. In addressing these challenges, the contributions of this thesis are to (i) demonstrate that individual control can improve performance in cilia-based devices, (ii) present accurate nonlinear models for pre- dicting the static response, and (iii) develop a machine-learning-based system identification and control strategy for output tracking

Serum amyloid A induces G-CSF expression and neutrophilia via Toll-like receptor 2

The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory diseases; however, its precise role in inflammation and infection, which often result in neutrophilia, remains ambiguous. In this study, we demonstrate that SAA is a potent endogenous stimulator of granulocyte colony-stimulated factor (G-CSF), a principal cytokine-regulating granulocytosis. This effect of SAA is dependent on Toll-like receptor 2 (TLR2). Our data demonstrate that, in mouse macrophages, both G-CSF mRNA and protein were significantly increased after SAA stimulation. The induction of G-CSF was blocked by an anti-TLR2 antibody and markedly decreased in the TLR2-deficient macrophages. SAA stimulation results in the activation of nuclear factor–κB and binding activity to the CK-1 element of the G-CSF promoter region. In vitro reconstitution experiments also support that TLR2 mediates SAA-induced G-CSF expression. In addition, SAA-induced secretion of G-CSF was sensitive to heat and proteinase K treatment, yet insensitive to polymyxin B treatment, indicating that the induction is a direct effect of SAA. Finally, our in vivo studies confirmed that SAA treatment results in a significant increase in plasma G-CSF and neutrophilia, whereas these responses are ablated in G-CSF– or TLR2-deficient mice