ISNI: 0000000121581279 , 000000040617962X
FundRef: 501100007242
The project WhyBehindScenes aims at developing new methods for automatically understanding the storyline in videos, and in particular the why behind the scenes in edited videos (films and TV shows). This will be investigated in two directions: first, by automatically understanding the storyline by focusing on the timeline, parts that are crucial for a plot, and correlation of scenes; second, by identifying the filmmaker’s decisions and integrating them in the video analysis by extracting the film’s signature (the style of the direction, the emotion a scene is conveying) and by creating novel sequences with specific directorial style. WhyBehindScenes targets to build systems capable of converting videos to books, by including not only the audio-visual information present in scenes but also the motivation, intention or even emotion behind events.
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FERMIcQED aims at interfacing novel quantum materials with microwave light at the level of the single photon and fermion. To achieve this ambitious goal, I plan to use low-dimensional quantum conductors – such as carbon nanotubes or semiconducting nanowires – combined with state-of-the-art architectures and techniques of circuit Quantum Electrodynamics. The idea consists in isolating an individual fermionic degree of freedom within a hybrid Josephson junction – a quantum dot connected to two superconductors. Due to the superconducting proximity effect, entangled electron-hole states – called the Andreev bound states – form in the quantum dot and depend on the superconducting phase difference. By enclosing the hybrid Josephson junction inside a superconducting photonic cavity, one can couple these fermionic states to microwave light and probe their quantum properties in a well-controlled environment. Specifically, FERMIcQED will tackle three key experiments. First, we will detect the spin degree of freedom of the Andreev bound states and manipulate it coherently as a superconducting spin qubit. We will demonstrate strong coupling with cavity photons, which will enable quantum logic operations and long-range qubit interactions. Second, we will operate the hybrid Josephson junction in the topological regime in order to observe and manipulate Majorana fermions, thus implementing a topological qubit. At last, we will probe the joint entangled dynamics of bosonic and fermionic modes that coexist in hybrid Josephson junctions and simulate the spin-boson problem.
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The lungs are the primary organs of the respiratory system in humans and many animals, responsible for molecular exchanges between external air and internal blood through mechanical ventilation. It has an extraordinary complex architecture, with the inherent fractal structure of the bronchial and blood vessel trees, as well as the hierarchical structure of the parenchyma. Lung biomechanics has been extensively studied by physiologists, experimentally as well as theoretically, from the air flow, blood flow and tissue stress points of view, laying the ground for our current fundamental understanding of the relationship between function and mechanical behavior. However, many questions remain, notably in the intricate coupling between the multiple constituents, between the many phenomena taking place at different spatial and temporal scales in health and disease. For example, even for healthy lungs, there is no quantitative model allowing to link tissue-level and organ-level experimental material responses. These fundamental questions represent real clinical challenges, as pulmonary diseases are an important health burden. Interstitial lung diseases, for instance, affect several million people globally. Idiopathic Pulmonary Fibrosis, notably, a progressive form of interstitial lung diseases where some alveolar septa get thicker and stiffer while others get completely damaged, remains poorly understood, poorly diagnosed, and poorly treated, with a current median survival rate inferior to 5 years. It has, however, been hypothesized that a mechanical vicious cycle is in place within the parenchyma of IPF patients, where fibrosis and damage induce large stresses, which in turns favor fibrosis. The general goal of this project is twofold: (i) scientifically, to better understand pulmonary (solid) mechanics, from the alveolar scale to the organ in health and (IPF) disease; (ii) clinically, to improve diagnosis and prognosis of (IPF) patients through personalized computational modeling. More precisely, I propose to develop a many-scale model of the parenchymal biomechanics, at all relevant spatial scales from the alveolus to the organ, and at the temporal scales of the breathing cycle and fibrosis process. Different representations at successive spatial scales will be linked by a computational nonlinear homogenization strategy with a priori model reduction based on a neural network. The model will integrate the rather unique experimental data produced by Drs. Bel-Brunon and Trunfio-Sfarghiu from LaMCoS (INSA-Lyon), i.e., 30 microtomography images at alveolar scale, plus 10 inflation tests of lobules: microstructures will be extracted from the images and systematically analyzed, and model parameters will be estimated from the mechanical tests. The model will also integrate clinical-radiological data provided by Profs. Nunes and Brillet from Avicenne APHP Hospital, i.e., standard pulmonary function tests and thoracic computed tomography imaging on 10 IPF patients plus 5 normal lung controls: a pipeline to estimate observable model parameters from clinical data will be set up, and generic values will be defined for the remaining parameters. The model and estimation procedure will represent augmented diagnosis and prognosis tools for the clinicians. The project will be coordinated by Dr. Genet, who is currently an Assistant Professor in the Mechanics Department of École Polytechnique with research posting within the M?DISIM team, which belongs to both INRIA and the Solid Mechanics Laboratory of École Polytechnique/CNRS. Throughout the project he will be assisted by Drs. Chapelle and Moireau at INRIA/École Polytechnique, and maintain strong scientific collaborations with the LaMCoS at INSA-Lyon and Télécom-SudParis, as well as strong clinical collaborations with the Avicenne APHP Hospital and Hypoxia & Lung Laboratory of Paris XIII University/INSERM.
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Cell migration is a critical process for embryogenesis, immune cell function and wound healing as well as cancer progression. Most normal cells migrate by protruding the plasma membrane forward through actin polymerization. The formation of a protrusion requires activation of the small GTPase Rac1 that in turn activates the WAVE complex, which induces branched actin networks through the Arp2/3 complex. For efficient cell migration, membrane protrusion at the leading edge must be sustained. Conversely, cells need to retract membrane protrusion to stop cell migration or turn. The tight control of protrusion lifetime and directional persistence is thus critical to fine tune cell migration. At the molecular level, persistence is controlled by positive and negative feedback loops. However, only few of these feedback loops have been identified and almost none has been characterized, in particular in vivo. In a joint effort with two other labs, proteomic screens were used to identify proteins that interact with the WAVE complex and whose interaction is modulated by branched actin. Based on different selection criteria such as their role in actin dynamics in vitro, conservation in fish, and absence of in vivo data, I selected three candidates. I will unravel their in vivo function at different scales, from embryonic development, to cell migration, to membrane protrusion and cytoskeleton dynamics. Actin feedback loops regulating cell migration will be specifically dissected. To do so, I will take advantage of two complementary and well characterized cellular models: endodermal cells and prechordal plate cells. Endodermal cells perform a random walk, while prechordal plate cells exhibit a directed collective migration. This project, which relies on validated unbiased screens and well established cellular models and approaches, will provide new insights in our understanding of actin dynamics regulation and mechanisms that fine tune cell migration.
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