4 research outputs found

    Turbulent Friction Drag Reduction Using Electroactive Polymer Surfaces

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    Both experiments and numerical simulations have provided evidence that an initially fully developed two-dimensional boundary layer, subjected to a sudden spanwise forcing, exhibits a decrease of turbulent quantities such as the Reynolds shear stress, turbulent kinetic energy and turbulent friction drag. In past experiments and investigations, such forcing has traditionally been in the form of spanwise wall oscillations, spanwise travelling Lorentz forcing, superimposed spanwise pressure gradients and spanwise travelling waves of an inplane flexible wall. The aim of this work is to take the idea a step further and develop an active surface which locally executes the motions described above making such a system more readily deployable. Two surfaces were developed: both executing in-plane local oscillations with amplitude close to or larger than the mean streak spacing in a turbulent flow, but based on two different technologies, electroactive polymers in the dielectric form of actuation and electromagnetic motor forcing. The effect of these two surfaces was confined to wall-normal heights on the order of the linear sublayer of the turbulent boundary layer, and frequency and wavelength similar to those reported in literature. Extensive hot-wire measurements, some PIV measurements and direct measurement of friction drag using a bespoke drag balance are presented for the systematic variation of the relevant parameters for turbulent friction drag reduction. Electroactive polymers (EAP) are able to undergo relatively large deflections at high frequencies. Developments in the field of EAP such as static and dynamic characterisation of the EAP membranes in use in this work, development of robust electrodes and their characterisation, in-house manufacturing of thin silicone membranes and post-processing of pre-built silicone membranes are presented. Numerical studies of the optimum pre-strain values and of the optimum electrode to passive portions width ratios are presented. Actuator development techniques including EAP membrane pre-stretch in a bespoke jig, EAP membrane pre-conditioning to go past the Mullins' effect, electrode preparation procedure and deposition, and frame preparation are presented. Actuator characterisation results including analysis of multi-flash photographs and laser profilometer scans for in-plane and out-plane deflections at different frequencies are also presented

    Mechanosensitive ATP release in the lungs

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    L’ATP est bien connue pour son rôle de transporteur d'énergie à l’intérieur des cellules, mais en dehors de la cellule, elle agit en tant que molécule de signalisation extracellulaire. En se liant aux récepteurs purinergiques, l’ATP extracellulaire amorce la signalisation purinergique afin de réguler certains processus physiologiques et pathophysiologiques. Dans les poumons, l’ATP stimule la sécrétion de surfactant et promeut la clairance mucociliaire. Compte tenu du rôle critique de l’ATP extracellulaire dans les poumons, il est important de comprendre le mécanisme du relargage d’ATP cellulaire — la première étape de la signalisation purinergique. Parce que les forces mécaniques constituent le déclencheur principal du relargage d’ATP, cette thèse a pour but d’investiguer le(s) mécanisme(s) physiologique(s) et les sources cellulaires d’un tel relargage d’ATP mécanosensible. Cet ouvrage est divisé en trois parties : 1) Pour étudier les caractéristiques spatiales et temporelles du relargage d’ATP, j’ai développé une technique d’imagerie hautement sensible basée sur la bioluminescence de la luciférine-luciférase couplée avec un système de lentilles à grand champ de vision (WFOV, wide field of view) optimisant l’apport de lumière. Pour évaluer notre approche d’imagerie, j’ai soumis des cellules A549, dérivées d’un adénocarcinome pulmonaire humain, à un étirement ou un choc hypotonique de 50% pour déclencher un relargage d’ATP. J’ai démontré que notre technique nous permet de quantifier précisément la quantité et le taux (ou l’efflux) d’ATP s’échappant des cellules. Le WFOV constitue un outil essentiel utilisé dans les études décrites dans cette thèse pour déterminer le mécanisme et la source cellulaire du relargage d’ATP dans l’alvéole. 2) Afin d’examiner le mécanisme physiologique du relargage d’ATP induit par l’étirement dans les cellulaires alvéolaires primaires, j’ai déterminé les contributions individuelles des cellules alvéolaires de type 1 (AT1) en comparaison des cellules alvéolaires de type 2 (AT2). Pour ce faire, des cellules AT2 fraîchement isolées de poumons de rats ont été ensemencées sur une chambre flexible en silicone et cultivées jusqu’à sept jours, ce qui permettait aux cellules AT2 de se transdifférencier progressivement en cellules semblables aux cellules AT1. Le ratio des cellules alvéolaires (AT2:AT1), étant de 4:1 au jour 3, est devenu 1:4 au jour 7. La quantité d'ATP libérée diminuait avec le nombre décroissant de cellules AT2, les impliquant en tant que principale source pour le relargage d’ATP en réponse à un étirement. Alors que les modulateurs pharmacologiques des canaux d’ATP, carbenoxolone et probénécide, ne diminuaient pas la quantité d’ATP libérée, le BAPTA, un chélateur de calcium intracellulaire ([Ca2+]i), l’a significativement réduite. De même, ces trois modulateurs exercent des effets similaires sur les réponses calciques intracellulaires mesurées par le Fura-2, suggérant une connexion entre le relargage d’ATP et les niveaux de [Ca2+]i. 3) Pour explorer le rôle qu’ont les propriétés viscoélastiques de la membrane dans le relargage d’ATP mécanosensible, j’ai démontré qu’une déformation de 30% induisait un relargage d’ATP transitoire qui était accompagné d’une absorption d’iodure de propidium (PI, propidium iodide) chez des cellules AT2. Ceci est cohérent avec une rupture membranaire transitoire induite par une déformation, assez large pour le passage d’ATP et de PI. L’efflux d’ATP augmente aussi selon le taux de déformation, et la durée de déformation prolonge la demi-vie du relargage d’ATP. Donc, ces résultats fournissent des indices sur la manière dont l’étirement de la membrane viscoélastique peut mener au relargage d’ATP par un mécanisme alternatif impliquant une mécanoporation de la membrane cellulaire. Dans l’ensemble, ces résultats démontrent que le relargage d’ATP ne se produit pas à travers les canaux conduisant l’ATP mais plutôt par une mécanoporation transitoire de la membrane. D’autres études sur les dommages membranaires sont nécessaires pour mieux comprendre sa contribution dans le relargage d’ATP mécanosensible et les signaux de [Ca2+]i. De telles études élucideront la signalisation purinergique dans les organes qui sont constamment exposés à des contraintes physiques. Ceci pourrait suggérer des cibles/approches thérapeutiques pour moduler les impacts négatifs d’un relargage d’ATP excessif observés lors de certaines conditions pathologiques, telles que les lésions pulmonaires induites par la ventilation mécanique.ATP is widely known to be an energy carrier within cells, but outside of the cell, it acts as an extracellular signaling molecule. Upon binding to purinergic receptors, extracellular ATP initiates the purinergic signaling to regulate certain physiological and pathophysiological processes. In the lungs, ATP stimulates surfactant secretion and promotes mucociliary clearance. Given the critical role of extracellular ATP in the lungs, it is important to understand the mechanism of cellular ATP release — the first step of purinergic signaling. Because mechanical forces constitute the primary trigger of ATP release, this thesis aims to investigate the physiological mechanism(s) and cellular sources of such mechanosensitive ATP release. This work is divided into three parts: 1) To study the spatial and temporal characteristics of ATP release, I developed a highly sensitive imaging technique based on luciferin-luciferase bioluminescence coupled with a custom-designed lens system, which combined a wide field of view (WFOV) and high light-gathering power. To evaluate our imaging approach, I subjected A549 cells, derived from human lung adenocarcinoma, to stretch or 50% hypotonic shock to trigger ATP release. I demonstrated that our technique allows us to precisely quantify the amount and the rate (or efflux) of ATP escaping from cells. The WFOV constitutes an essential tool used in the studies described in this thesis to determine the mechanism and cellular source of ATP release in the alveolus. 2) To examine the physiological mechanism of stretch-induced ATP release in primary alveolar cells, I determined the individual contributions of alveolar type 1 (AT1) in comparison with alveolar type 2 (AT2) cells. To this end, freshly isolated AT2 cells from rat lungs were seeded on a flexible silicone chamber and were cultured for up to seven days, which allowed AT2 cells to progressively transdifferentiate into AT1-like cells. The ratio of alveolar cells (AT2:AT1), being 4:1 on day 3, became 1:4 on day 7. The quantity of released ATP decreased with the decreasing numbers of AT2 cells, implicating them as the main source of ATP release in response to stretch. While pharmacological ATP channel modulators, carbenoxolone and probenecid, did not diminish the amount of ATP release, BAPTA, an intracellular calcium ([Ca2+]i) chelator, significantly reduced it. Likewise, these three modulators had similar effects on intracellular calcium responses measured by Fura-2, suggesting a connection between ATP release and [Ca2+]i levels. 3) To explore the role of membrane viscoelastic properties in mechanosensitive ATP release, I demonstrated that a 30% strain induced transient ATP release that was accompanied by uptake of propidium iodide (PI) in AT2 cells. This is consistent with a strain-induced transient membrane rupture, big enough for the passage of ATP and PI. ATP efflux also increases with strain rate, and hold time prolongs the half-life of ATP release. Thus, these results provide clues on how stretching of the viscoelastic membrane may lead to ATP release via an alternate mechanism involving transient mechanoporation of the cell membrane. Overall, these findings demonstrate that stretch-induced ATP release does not occur through ATP-conducting channels but rather a transient membrane mechanoporation. Further studies on membrane injury induced by strain are needed to better understand its contribution to mechanosensitive ATP release and [Ca2+]i signaling. Such studies will elucidate purinergic signaling in organs that are constantly exposed to physical stresses. This could suggest novel therapeutic targets/approach to modulate the negative impacts of excessive ATP release observed under certain pathological conditions, such as ventilator-induced lung injury

    Business Model Innovation in the Aerospace Industry: Strategic Options for Maintenance, Repair, and Overhaul Firms

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    Aircraft Maintenance, Repair, and Overhaul (MRO) is a $76bn industry in which established service firms such as Lufthansa Technik, Delta Tech Ops, and AFI KLM Engineering & Maintenance come under increasing competitive pressure by aircraft, engine, and system manufacturers such as Rolls-Royce, Airbus, and Thales. Increasing price pressure on asset sales and the opportunity to generate profitable service-based revenue streams in the aftermarket makes servitization an imperative for manufacturers, who pursue this type of Business Model Innovation (BMI) aggressively. Traditional MRO service firms do not only play a vital role for shareholders and employees but also let airlines benefit from competition in a contracting MRO market that is in danger of being monopolized. Furthermore, MRO services represent 15-18% of airlines’ direct operating costs (compared to 8% for aircraft financing) and are paramount to ensure safe, reliable, and punctual airline operations. This study explores how MROs can successfully innovate their business model when faced with competition from manufacturers that offer product-service bundles to their customers. While academia has made significant advancements on how manufacturers can successfully add services to their business model, we know very little about how traditional service firms can navigate in such a servitized environment. By conducting three case studies based on 50 in-depth interviews with MRO and airline managers, I identify a portfolio of four business model configurations that MROs can employ to offer solutions and create value in solution networks. My findings indicate that MROs can use a contingency-based approach to innovate their business model through solution-specific and relational dynamic capabilities. When competing with manufacturers, MROs can gain a competitive advantage by leveraging the unique elements of their service-based business model. However, when alliancing is the more promising option, MROs need to innovate their business model to successfully add and appropriate value in these complex, coopetitive relationships. My intention is to make three academic contributions: The principal contribution is clarifying the role of pure service firms in servitization research and the development of strategic options for MROs to cope with servitization practices of manufacturers through business model innovation. Second, this study takes a first step in unveiling the “dark side of servitization”, uncovering the currently obscure less favorable aspects of this phenomenon. Third, I outline business models of MRO firms that have been overlooked in the efforts of describing changing airlines’ and manufacturers’ business models, even though they represent a central link in the supply chain. This study also claims to make three managerial contributions: first, managers of MROs can make use of the findings to drive the innovation of their business model and ensure long-term competitiveness when faced with servitization. Second, the results inform airline managers about significant environmental changes in the MRO market relevant for technical airline operations, make-or-buy decisions, and MRO procurement. Third, aerospace manufacturers can benefit from the insights developed in this work to either build a positional advantage against MROs or rely on these specialized players to complement their service offers
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