Quasiparticle diffusion based heating in superconductor tunneling micro-coolers

In a hybrid Superconductor - Insulator - Normal metal tunnel junction biased just below the gap, the extraction of hot electrons out of the normal metal results in electronic cooling effect. The quasiparticles injected in the superconductor accumulate near the tunnel interface, thus increasing the effective superconductor temperature. We propose a simple model for the diffusion of excess quasiparticles in a superconducting strip with an additional trap junction. This diffusion model has a complete analytic solution, which depends on experimentally accessible parameters. We find that the accumulated quasiparticles near the junction reduce the efficiency of the device. This study is also relevant to more general situations making use of superconducting tunnel junctions, as low temperature detectors.Comment: 4 pages, 3 figure

Long-range coherence and mesoscopic transport in N-S metallic structures

We review the mesoscopic transport in a diffusive proximity superconductor made of a normal metal (N) in metallic contact with a superconductor (S). The Andreev reflection of electrons on the N-S interface is responsible for the diffusion of electron pairs in N. Superconducting-like properties are induced in the normal metal. In particular, the conductivity of the N metal is locally enhanced by the proximity effect. A re-entrance of the metallic conductance occurs when all the energies involved (e.g. temperature and voltage) are small. The relevant characteristic energy is the Thouless energy which is $\hbar$ divided by the diffusion time for an electron travelling throughout the sample. In loop-shaped devices, a 1/T temperature-dependent oscillation of the magnetoresistance arises with a large amplitude from the long-range coherence of low-energy pairs.Comment: Review paper, 13 pages with 5 included epsf figures, to appear in Superlattices and Microstructures, minor change

Chronic hypoxia aggravates monocrotaline-induced pulmonary arterial hypertension: a rodent relevant model to the human severe form of the disease

International audienc

Impairment of NO-Dependent Relaxation in Intralobar Pulmonary Arteries: Comparison of Urban Particulate Matter and Manufactured Nanoparticles

International audienceBACKGROUND AND OBJECTIVES: Because pulmonary circulation is the primary vascular target of inhaled particulate matter (PM), and nitric oxide is a major vasculoprotective agent, in this study we investigated the effect of various particles on the NO-cyclic guanosine monophosphate (cGMP) pathway in pulmonary arteries. METHODS: We used intrapulmonary arteries and/or endothelial cells, either exposed in vitro to particles or removed from PM-instilled animals for assessment of vasomotricity, cGMP and reactive oxygen species (ROS) levels, and cytokine/chemokine release. RESULTS: Endothelial NO-dependent relaxation and cGMP accumulation induced by acetylcholine (ACh) were both decreased after 24 hr exposure of rat intrapulmonary arteries to standard reference material 1648 (SRM1648; urban PM). Relaxation due to NO donors was also decreased by SRM1648, whereas responsiveness to cGMP analogue remained unaffected. Unlike SRM1648, ultrafine carbon black and ultrafine and fine titanium dioxide (TiO2) manufactured particles did not impair NO-mediated relaxation. SRM1648-induced decrease in relaxation response to ACh was prevented by dexamethasone (an anti-inflammatory agent) but not by antioxidants. Accordingly, SRM1648 increased the release of proinflammatory mediators (tumor necrosis factor-alpha, interleukin-8) from intrapulmonary arteries or pulmonary artery endothelial cells, but did not elevate ROS levels within intrapulmonary arteries. Decreased relaxation in response to ACh was also evidenced in intrapulmonary arteries removed from rats intratracheally instilled with SRM1648, but not with fine TiO2. CONCLUSION: In contrast to manufactured particles (including nanoparticles), urban PM impairs NO but not cGMP responsiveness in intrapulmonary arteries. We attribute this effect to oxidative-stress-independent inflammatory response, resulting in decreased guanylyl cyclase activation by NO. Such impairment of the NO pathway may contribute to urban-PM-induced cardiovascular dysfunction