Supratransmission et bistabilité nonlinéaire dans<br />les milieux à bandes interdites photoniques et électroniques

We study wave scattering in different nonlinear media possessing a natural forbidden band gap. In particular, we show the existence of a bistable behavior in media governed by the sine-Gordon equation (short pendula chain, Josephson junction array, quantum Hall bilayer), or the nonlinear Schroedinger equation (Kerr and Bragg media), in discrete and continous models. These different media are submitted to periodic boundary conditions with a frequency in the forbidden band gap and an amplitude that determines their stability states. Indeed, for a sufficient amplitude (supratransmission), the medium switches from reflector to transmittor, hence allowing the output signal to jump from evanescent to large values. We give a complete analytical description of the bistability that allows to understand the different stationnary states observed and to predict the switch of one state to the other.On étudie, dans cette thèse, la diffusion d'ondes dans différents milieux nonlinéaires possédant une bande interdite naturelle. On montre, en particulier, l'existence d'un comportement de bistabilité dans les milieux régis, soit par l'équation de sine-Gordon (chaîne de pendules courte, réseaux de jonctions Josephson, double couches à effet Hall quantique), soit par l'équation de Schrödinger nonlinéaire (milieu Kerr et milieu de Bragg), dans les cas discrets et continus. Ces différents milieux sont soumis à des conditions aux bords périodiques, dont la fréquence est prise dans la bande interdite et avec une amplitude déterminant l'état de stabilité du système. En effet, pour une amplitude suffisante (supratransmission), le milieu n'est plus réfléchissant et absorbe de l'énergie, faisant passer le signal de sortie d'un état d'amplitude évanescente vers un état de très grande amplitude. On donne, par ailleurs, une description analytique complète de la bistabilité qui permet de comprendre les différents états stationnaires observés dans ces milieux et de prédire le passage d'un état à un autre

Theory of a Josephson junction parallel array detector sensitive to very weak signals

An array of coupled short junctions (Josephson junction parallel array) is shown to be able to response to ultra-weak signals when it is worked at the onset of nonlinear supratransmission in the hysteresis loop of bistability. The theory is based on the fundamental solutions of the continuous limit (the sine-Gordon equation on the finite interval submitted to Neuman boundary conditions) that result from synchronization and adaptation to the external driving. This provides the solution to a problem that dates back to 1986 [O. H. Olsen and M. R. Samulsen, Phys. Rev. B34, 3510 (1986)], namely the complete analytical understanding of the bistability in a long Josephson junction or in an array of short junctions. The property allows to conceive ultrasensitive detectors or else, by convenient modulation of the seed, efficient digital amplifiers. Numerical simulations reveal that such a bistable behavior occurs also in two-dimensional lattices where no theory is available yet

Quantum Hall bilayer digital amplifier

A quantum Hall double layer system at total Landau level filling factor ν=1, seeded by a modulated ac-voltage input signal of frequency inside the forbidden band gap, is demonstrated to work as a digital amplifier of ultra weak signals. The theory employs to the sine-Gordon model and it is confirmed by the first experimental observations of nonlinear bistable transmission in a pendula chain. Copyright EDP Sciences/Società Italiana di Fisica/Springer-Verlag 2006

Bistable Transmitting Nonlinear Directional Couplers

Nonlinearity induced by intensity-dependent refractive indices (Kerr media) can be used as a means to conceive light detectors sensitive to very weak excitation. This property results from the bistability properties of the nonlinear SchrÄodinger equation submitted to boundary value data on the finite interval. The detector is obtained by coupling two single 1D waveguide to a 2D slab waveguide with adjusted indices. The resulting device then presents unusual light propagation properties and in particular may switch from almost vanishing to intense output under excitation by a weak signal

Frequency divider by underdamped Josephson transmission line

74.50.+r Tunneling phenomena; point contacts, weak links, Josephson effects, 05.45.Yv Solitons, 74.81.Fa Josephson junction arrays and wire networks,

Liver X Receptor β activation induces pyroptosis of human and murine colon cancer cells

International audienceLiver X receptors (LXRs) have been proposed to have some anticancer properties, through molecular mechanisms that remain elusive. Here we report for the first time that LXR ligands induce caspase-1-dependent cell death of colon cancer cells. Caspase-1 activation requires Nod-like-receptor pyrin domain containing 3 (NLRP3) inflammasome and ATP-mediated P2 × 7 receptor activation. Surprisingly, LXRβ is mainly located in the cytoplasm and has a non-genomic role by interacting with pannexin 1 leading to ATP secretion. Finally, LXR ligands have an antitumoral effect in a mouse colon cancer model, dependent on the presence of LXRβ, pannexin 1, NLRP3 and caspase-1 within the tumor cells. Our results demonstrate that LXRβ, through pannexin 1 interaction, can specifically induce caspase-1-dependent colon cancer cell death by pyroptosis

Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the Nlrp3 inflammasome and promotes tumor growth

International audienceChemotherapeutic agents are widely used for cancer treatment. In addition to their direct cytotoxic effects, these agents harness the host's immune system, which contributes to their antitumor activity. Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1β (IL-1β), which curtails anticancer immunity. Chemotherapy-triggered IL-1β secretion relied on lysosomal permeabilization and the release of cathepsin B, which bound to Nlrp3 and drove caspase-1 activation. MDSC-derived IL-1β induced secretion of IL-17 by CD4+ T cells, which blunted the anticancer efficacy of the chemotherapy. Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3−/− or Casp1−/− mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Altogether, these results identify how activation of the Nlrp3 inflammasome in MDSCs by 5FU and Gem limits the antitumor efficacy of these chemotherapeutic agents