Experimental Flight Testing of an Adaptive Autopilot with Parameter Drift Mitigation

This paper modifies an adaptive multicopter autopilot to mitigate instabilities caused by adaptive parameter drift and presents simulation and experimental results to validate the modified autopilot. The modified adaptive controller is obtained by including a static nonlinearity in the adaptive loop, updated by the retrospective cost adaptive control algorithm. It is shown in simulation and physical test experiments that the adaptive autopilot with proposed modifications can continually improve the fixed-gain autopilot as well as prevent the drift of the adaptive parameters, thus improving the robustness of the adaptive autopilot.Comment: 6 pages, 16 figures, submitted to IROS 202

Optimizing the buckling characteristics and weight of functionally graded circular plates using the multi-objective Pareto archived simulated annealing algorithm (PASA)

In this study for the first time, weight and critical buckling load in two kinds of functionally graded (FG) circular plates, namely, aluminum–alumina of (Al/Al2O3) and aluminum–zirconia (Al/ZnO2), are optimized using multi-objective Pareto archived simulated annealing algorithm (PASA). Material properties are assumed to vary with the power law in terms of the volume fractions of the constituent in two forms of symmetric and asymmetric with respect to the middle surface. The plate is subjected to uniform radial load and is considered for two boundary conditions, namely, simply supported and clamped edges. Aim at obtaining the Pareto archive is to achieve simultaneously the maximum buckling and the minimum weight concerning with proposed constraints. The parameters include the radius, thickness and volume fraction that the certain range is intended individually. The constraints are presented in form of the ratio of thickness to radius in category of the thin plates as well as the critical buckling stress being in the elastic range. Proposed simulated annealing algorithm is coded in MATLAB to obtain optimal non-dominated solution

Increasing Viral Dose Causes a Reversal in CD8(+) T Cell Immunodominance during Primary Influenza Infection due to Differences in Antigen Presentation, T Cell Avidity, and Precursor Numbers

Fulltext embargoed for: 12 months post date of publicationT cell responses are characterized by the phenomenon of immunodominance (ID), whereby peptide-specific T cells are elicited in a reproducible hierarchy of dominant and subdominant responses. However, the mechanisms that give rise to ID are not well understood. We investigated the effect of viral dose on primary CD8(+) T cell (T(CD8+)) ID by injecting mice i.p. with various doses of influenza A virus and assessing the primary T(CD8+) response to five dominant and subdominant peptides. Increasing viral dose enhanced the overall strength of the T(CD8+) response, and it altered the ID hierarchy: specifically, NP(366-374) T(CD8+) were dominant at low viral doses but were supplanted by PA(224-233) T(CD8+) at high doses. To understand the basis for this reversal, we mathematically modeled these T(CD8+) responses and used Bayesian statistics to obtain estimates for Ag presentation, T(CD8+) precursor numbers, and avidity. Interestingly, at low viral doses, Ag presentation most critically shaped ID hierarchy, enabling T(CD8+) specific to the more abundantly presented NP(366-374) to dominate. By comparison, at high viral doses, T(CD8+) avidity and precursor numbers appeared to be the major influences on ID hierarchy, resulting in PA(224-233) T(CD8+) usurping NP(366-374) cells as the result of higher avidity and precursor numbers. These results demonstrate that the nature of primary T(CD8+) responses to influenza A virus is highly influenced by Ag dose, which, in turn, determines the relative importance of Ag presentation, T(CD8+) avidity, and precursor numbers in shaping the ID hierarchy. These findings provide valuable insights for future T(CD8+)-based vaccination strategies

Nonlinear Buckling Analysis of Cylindrical Nanoshells Conveying Nano-Fluid in Hygrothermal Environment

The present work addresses the critical buckling of circular cylindrical nano-shells containing static/dynamic nanofluids under the influence of different thermal fields that can also lead to appear the effect of thermal moisture so-called hygrothermal forces fields. To this end, the classical Sanders theory of cylindrical plates and shells is generalized by utilizing the non-classical nonlocal elasticity theory to derive the modified dynamic equations governing the nanofluid-nanostructure interaction (nano-FSI) problem. Then, the dimensionless obtained equations are analytically solved using the energy method. Herein, the applied nonlinear heat and humidity fields are considered as three types of longitudinal, circumferential, and simultaneously longitudinal-circumferential forces fields. The mentioned cases are examined separately for both high- and room-temperatures modes. The results show a significant effect of nanofluid passing through the nanostructure and its velocity on the critical buckling strain of the nano-systems, especially at high temperatures

An optimized method for establishing high purity murine CD8+ T cell cultures.

Establishing CD8(+) T cell cultures has been empirical and the published methods have been largely individual laboratory based. In this study, we optimized culturing conditions and show that IL-2 concentration is the most critical factor for the success of establishing CD8(+) T cell cultures. High IL-2 concentration encouraged T cells to non-specifically proliferate, express a B cell marker, B220, and undergo apoptosis. These cells also lose typical irregular T cell morphology and are incapable of sustaining long-term cultures. Using tetramer and intracellular cytokine assessments, we further demonstrated that many antigen-specific T cells have been rendered nonfunctional when expanded under high IL-2 concentration. When IL-2 is used in the correct range, B220-mediated cell depletion greatly enhanced the success rate of such T cell cultures

Host CD8α+ and CD103+ dendritic cells prime transplant antigen-specific CD8+ T cells via cross-dressing

The participation of dendritic cells (DCs) in CD8+ T-cell-mediated allograft rejection is a long-standing question of great clinical relevance for tissue transplantation. Here, we show that Batf3-/- mice demonstrate delayed allo-skin graft rejection and are deficient in priming allo-specific CD8+ T cells. Batf3-/- mouse priming is restored by transferring either purified CD8α+ or CD103+ DCs, demonstrating the critical role of these cells in alloreactivity. Using Db -restricted antiviral F5 transgenic T-cell receptor T cells, which we demonstrate are alloreactive with H-2Kd , we show that cross-dressing of CD8α+ and CD103+ primes CD8+ T-cell or allo-specific responses in vitro and in vivo. These findings suggest novel strategies for moderating tissue rejection based on interfering with DC cross-dressing or subsequent interaction with T cells

Monocyte apoptotic bodies are vehicles for influenza A virus propagation

The disassembly of apoptotic cells into small membrane-bound vesicles termed apoptotic bodies (ApoBDs) is a hallmark of apoptosis; however, the functional significance of this process is not well defined. We recently discovered a new membrane protrusion (termed beaded apoptopodia) generated by apoptotic monocytes which fragments to release an abundance of ApoBDs. To investigate the function of apoptotic monocyte disassembly, we used influenza A virus (IAV) infection as a proof-of-concept model, as IAV commonly infects monocytes in physiological settings. We show that ApoBDs generated from IAV-infected monocytes contained IAV mRNA, protein and virions and consequently, could facilitate viral propagation in vitro and in vivo, and induce a robust antiviral immune response. We also identified an antipsychotic, Haloperidol, as an unexpected inhibitor of monocyte cell disassembly which could impair ApoBD-mediated viral propagation under in vitro conditions. Together, this study reveals a previously unrecognised function of apoptotic monocyte disassembly in the pathogenesis of IAV infections