1,325 research outputs found
Relaxation approximation of Friedrich's systems under convex constraints
This paper is devoted to present an approximation of a Cauchy problem for
Friedrichs' systems under convex constraints. It is proved the strong
convergence in L^2\_{loc} of a parabolic-relaxed approximation towards the
unique constrained solution
Experimental realization of an ideal Floquet disordered system
The atomic Quantum Kicked Rotor is an outstanding "quantum simulator" for the
exploration of transport in disordered quantum systems. Here we study
experimentally the phase-shifted quantum kicked rotor, which we show to display
properties close to an ideal disordered quantum system, opening new windows
into the study of Anderson physics.Comment: 10 pages, 7 figures, submitted to New Journal of Physics focus issue
on Quantum Transport with Ultracold Atom
Controlling symmetry and localization with an artificial gauge field in a disordered quantum system
Anderson localization, the absence of diffusion in disordered media, draws
its origins from the destructive interference between multiple scattering
paths. The localization properties of disordered systems are expected to be
dramatically sensitive to their symmetry characteristics. So far however, this
question has been little explored experimentally. Here, we investigate the
realization of an artificial gauge field in a synthetic (temporal) dimension of
a disordered, periodically-driven (Floquet) quantum system. Tuning the strength
of this gauge field allows us to control the time-reversal symmetry properties
of the system, which we probe through the experimental observation of three
symmetry-sensitive `smoking-gun' signatures of localization. The first two are
the coherent backscattering, marker of weak localization, and the coherent
forward scattering, genuine interferential signature of Anderson localization,
observed here for the first time. The third is the direct measurement of the
scaling function in two different symmetry classes, allowing to
demonstrate its universality and the one-parameter scaling hypothesis
Trusting Computations: a Mechanized Proof from Partial Differential Equations to Actual Program
Computer programs may go wrong due to exceptional behaviors, out-of-bound
array accesses, or simply coding errors. Thus, they cannot be blindly trusted.
Scientific computing programs make no exception in that respect, and even bring
specific accuracy issues due to their massive use of floating-point
computations. Yet, it is uncommon to guarantee their correctness. Indeed, we
had to extend existing methods and tools for proving the correct behavior of
programs to verify an existing numerical analysis program. This C program
implements the second-order centered finite difference explicit scheme for
solving the 1D wave equation. In fact, we have gone much further as we have
mechanically verified the convergence of the numerical scheme in order to get a
complete formal proof covering all aspects from partial differential equations
to actual numerical results. To the best of our knowledge, this is the first
time such a comprehensive proof is achieved.Comment: N° RR-8197 (2012). arXiv admin note: text overlap with
arXiv:1112.179
Caractérisation de la voie d'activation des interférons de type I
Codirecteur de recherche: Dr Sylvain MelocheDurant ces quatre derniĂšres annĂ©es, le champ de recherche concernant lâimmunitĂ© innĂ©e a grandement Ă©tĂ© influencĂ© par la dĂ©couverte des IKK-related kinases, TBK1 et IKKi, deux kinases rĂ©gulant lâactivitĂ© des facteurs de transcription IRF-3/IRF-7 et NF-ÎșB. Les kinases TBK1 and IKKi furent notamment dĂ©montrĂ©es comme Ă©tant responsables de la phosphorylation en C-terminal de IRF-3. Toutefois, lâidentitĂ© des sites phosphoaccepteurs ciblĂ©s par ces kinases restait un sujet de controverse. En combinant la spectromĂ©trie de masse aux essais de phosphorylation in vitro de His-IRF-3 par la kinase recombinante TBK1, nous dĂ©montrons que les sĂ©rines 396 et 402 sont directement phosphorylĂ©es par cette kinase. Nos analyses biochimiques rĂ©vĂšlent Ă©galement que la mutation S396A, localisĂ©e dans le cluster II, abolit lâhomodimĂ©risation, lâassociation Ă CBP et lâaccumulation nuclĂ©aire de IRF-3. De façon intĂ©ressante, la mutation de la sĂ©rine 339, impliquĂ©e dans la stabilitĂ© de IRF-3, provoque Ă©galement une perte dâassociation Ă CBP et de la dimĂ©risation du facteur de transcription sans toutefois affecter la transactivation des gĂšnes antiviraux en autant que la sĂ©rine 396 soit disponible pour accepter un Ă©vĂ©nement de phosphorylation. Nos expĂ©riences de complĂ©mentation de MEFs IRF-3 KO rĂ©vĂšlent la prĂ©sence dâun mĂ©canisme compensatoire impliquant la sĂ©rine 339 et la sĂ©rine 396 dans lâinduction des IFN-stimulated genes (ISGs), ISG56 and ISG54. Globalement, les donnĂ©es prĂ©sentĂ©es dans cette Ă©tude nous ont permis de reconsidĂ©rer le modĂšle dâactivation du facteur de transcription IRF-3 actuellement proposĂ© et dây ajouter certaines subtilitĂ©s.
TRAF3 est Ă©galement un mĂ©diateur central impliquĂ© dans lâinduction de la rĂ©ponse interfĂ©ron de type I. Cette fois, en couplant la spectromĂ©trie de masse Ă la technique de purification protĂ©ique par affinitĂ©, nous avons identifiĂ© Sec16A et p115, deux protĂ©ines du systĂšme de transport vĂ©siculaire ER-Golgi , comme Ă©tant des nouveaux partenaires protĂ©iques de Flag-TRAF3. Nos expĂ©riences dĂ©montrent la localisation cellulaire de TRAF3 au niveau du systĂšme de transport vĂ©siculaire. De plus, la diminution des niveaux dâexpression de p115 ou Sec16A provoque une redistribution cellulaire de TRAF3 et affecte la rĂ©ponse interfĂ©ron suivant une stimulation par de lâARN double brin. Nos rĂ©sultats dĂ©montrent Ă©galement une colocalisation de TRAF3 et TRADD au niveau du cis-Golgi ainsi quâune interaction avec la protĂ©ine du translocon Sec61ÎČ mĂ©diĂ©e par lâintermĂ©diaire de Sec5. De façon gĂ©nĂ©rale, nos donnĂ©es suggĂšrent que la localisation cellulaire de TRAF3 au niveau des compartiments de transport vĂ©siculaire est requise afin dâobtenir une rĂ©ponse antiviral optimale par la voie de signalisation cellulaire associĂ©e aux RIG-I-like RNA helicases, RIG-I et MDA5. Nos donnĂ©es appuient Ă©galement le rĂŽle potentiel prĂ©cĂ©demment suggĂ©rĂ© de lâexocyste dans lâĂ©tablissement dâune rĂ©ponse antivirale.Over the past four years, the field of the innate immune response has been highly influenced by the discovery of the IÎșB kinase (IKK)-related kinases, TBK1 and IKKi, which regulate the activity of IRF-3/IRF-7 and NF-ÎșB transcription factors. The IKK-related kinases, TBK1 and IKKi, were recently shown to be responsible for the C-terminal phosphorylation of IRF-3. However, the identity of the phosphoacceptor site(s) targeted by these two kinases remains unclear. By combining mass spectrometry analysis to in vitro kinase assays using full length His-IRF3 as a substrate, we have demonstrated that serine 402 and serine 396 were directly targeted by TBK1. Analysis of Ser/Thr to Ala mutants revealed that S396A mutation, located in cluster II, abolished IRF-3 homodimerization, CBP association and nuclear accumulation. Interestingly, mutation of serine 339, which is involved in IRF-3 stability, also abrogated CBP association and dimerization without affecting gene transactivation as long as serine 396 remained available for phosphorylation. Complementation of MEFs IRF-3 KO also reveals a compensatory mechanism of serine 339 and serine 396 in the ability of IRF-3 to induce IFN-stimulated genes (ISGs) ISG56 and ISG54 expression. These data lead us to reconsider the current model of IRF-3 activation.
TRAF3 is also a central mediator that is important for inducing type I interferon production in response to intracellular double-stranded RNA. By combining Flag-Affinity purification using Flag-TRAF3 as a bait to mass spectrometry, we have identified Sec16A and p115, two proteins of the ER-to-Golgi vesicular transport system, as novel TRAF3 interactors. We found that TRAF3 localizes to the ER-to-Golgi vesicular pathway and behaves like a cis-Golgi protein. Depletion of p115 or Sec16A disrupts the cis-Golgi cellular localization of TRAF3 and affects type I Interferon response following double-stranded RNA treatment. Furthermore, we demonstrate that TRAF3 colocalizes with TRADD at the cis-Golgi and also interacts with the translocon protein Sec61ÎČ in a Sec5 dependent manner. Together, our data suggest that the cellular localization of TRAF3 to the ER-to-Golgi transport compartments is required for an optimal RIG-I-like Helicases (RLH)-Cardif-dependent antiviral immune response. Our findings also highlight the potential role of the exocyst in the innate immune response
Khalid Mouna, Catherine Terrien, LeĂŻla Bouasria, Ă©ds, Terrains marocains, sur les traces de chercheurs dâici et dâailleurs
Ce livre cherche Ă savoir comment des chercheurs marocains ou Ă©trangers ont abordĂ© leur terrain ethnographique au cours des derniĂšres dĂ©cennies au Maroc, en particulier aprĂšs 2000. Des recherches de plus ou moins longues durĂ©es sur des terrains (fieldworks) marocains existent depuis le xixe siĂšcle, mais une rĂ©flexion sur les procĂ©dures de contact et les stratĂ©gies utilisĂ©es par les chercheurs ne se dĂ©veloppent quâavec Paul Pascon dans les annĂ©es 1960, puis avec Paul Rabinow, un peu plus tard ..
Dark Optical Lattice of Ring Traps for Cold Atoms
We propose a new geometry of optical lattice for cold atoms, namely a lattice
made of a 1D stack of dark ring traps. It is obtained through the interference
pattern of a standard Gaussian beam with a counter-propagating hollow beam
obtained using a setup with two conical lenses. The traps of the resulting
lattice are characterized by a high confinement and a filling rate much larger
than unity, even if loaded with cold atoms from a MOT. We have implemented this
system experimentally, and obtained a lattice of ring traps populated with
typically 40 atoms per site with a life time of 30 ms. Applications in
statistical physics, quantum computing and Bose-Einstein condensate dynamics
are conceivable.Comment: 4 pages, submitted to PR
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