86 research outputs found
Ultra-coherent single photon source
We present a novel type of single photon source in solid state, based on the
coherent laser light scattering by a single InAs quantum dot. We demonstrate
that the coherence of the emitted single photons is tailored by the resonant
excitation with a spectral linewidth below the radiative limit. Our
ultra-coherent source opens the way for integrated quantum devices dedicated to
the generation of single photons with high degrees of indistinguishability
Approches transcriptomiques dans lâĂ©tude de la fibrose kystique
Les avancĂ©es en biotechnologie ont permis lâidentification dâun grand nombre
de mécanismes moléculaires, soulignant également la complexité de la
rĂ©gulation gĂ©nique. NĂ©anmoins, avoir une vision globale de lâhomĂ©ostasie
cellulaire, nous est pour lâinstant inaccessible et nous ne sommes en mesure
que dâen avoir quâune vue fractionnĂ©e. Ătant donnĂ© lâavancement des
connaissances des dysfonctionnements moléculaires observés dans les
maladies génétiques telles que la fibrose kystique, il est encore difficile de
produire des thérapies efficaces.
La fibrose kystique est causée par la mutation de gÚne CFTR (cystic fibrosis
transmembrane conductance regulator), qui code pour un canal chlorique
transmembranaire. La mutation la plus frĂ©quente (ÎF508) induit un repliement
incorrect de la protéine et sa rétention dans le réticulum endoplasmique.
Lâabsence de CFTR fonctionnel Ă la membrane a un impact sur lâhomĂ©ostasie
ionique et sur lâhydratation de la muqueuse respiratoire. Ceci a pour
conséquence un défaut dans la clairance mucocilliaire, induisant infection
chronique et inflammation excessive, deux facteurs fondamentaux de la
physiopathologie.
Lâinflammation joue un rĂŽle trĂšs important dans lâĂ©volution de la maladie et
malgrĂ© le nombre important dâĂ©tudes sur le sujet, la rĂ©gulation du processus
inflammatoire est encore trĂšs mal comprise et la place quây occupe le CFTR
nâest pas Ă©tablie.
Toutefois, plusieurs autres facteurs, tels que le stress oxydatif participent Ă la
physiopathologie de la maladie, et considérer leurs impacts est important pour
permettre une vision globale des acteurs impliqués.
Dans notre Ă©tude, nous exploitons la technologie des puces Ă ADN, pour
Ă©valuer lâĂ©tat transcriptionnel dâune cellule Ă©pithĂ©liale pulmonaire humaine
fibro-kystique.
Dans un premier temps, lâanalyse de notre expĂ©rience identifie 128 gĂšnes
inflammatoires sur-exprimés dans les cellules FK par rapport aux cellules non
FK oĂč apparaissent plusieurs familles de gĂšnes inflammatoires comme les
cytokines ou les calgranulines. Lâanalyse de la littĂ©rature et des annotations
suggĂšrent que la modulation de ces transcripts dĂ©pend de la cascade de NF-ÎșB
et/ou des voies de signalisation associées aux interférons (IFN). En outre, leurs
modulations pourraient ĂȘtre associĂ©es Ă des modifications Ă©pigĂ©nĂ©tiques de
leurs loci chromosomiques.
Dans un second temps, nous Ă©tudions lâactivitĂ© transcriptionnelle dâune cellule
épithéliale pulmonaire humaine FK en présence de DMNQ, une molécule
cytotoxique. Notre but est dâidentifier les processus biologiques perturbĂ©s par la
mutation du gÚne CFTR en présence du stress oxydatif.
Fondé sur une analyse canonique de redondance, nous identifions 60 gÚnes
associés à la mort cellulaire et leur variance, observée dans notre expérience,
sâexplique par un effet conjoint de la mutation et du stress oxydatif. La mesure
de lâactivitĂ© des caspases 3/7, des effecteurs de lâapoptose (la mort cellulaire
programmĂ©e), montre que les cellules porteuses de la mutation ÎF508, dans
des conditions de stress oxydatif, seraient moins apoptotiques que les cellules
saines. Nos données transcriptomiques suggÚrent que la sous-activité de la
cascade des MAPK et la sur-expression des gĂšnes anti-apoptotiques pourraient
ĂȘtre impliquĂ©es dans le dĂ©sĂ©quilibre de la balance apoptotique.Biotechnical advances have allowed a large number of molecular mechanisms
to be identified, and have also underlined the complexity of gene regulation.
Nonetheless, we still only have a partial understanding of cellular homeostasis.
Even with our current knowledge, molecular dysfunctionality observed in genetic
illnesses such as cystic fibrosis remain largely misunderstood, prohibiting us
from developing efficient treatments. Cystic fibrosis is caused by a mutation of
the CFTR (cystic fibrosis transmembrane conductance regulator) gene which
codes for a chloric transmembrane channel. The most frequent mutation
(ÎF508) causes the unfolding of the protein and its retention in the endoplasmic
reticulum. This absence of a functional CFTR to the membrane has an impact
on the ionic homeostasis and the hydration of the respiratory mucus.
Consequently, the mucociliary clearance is disrupted, which leads to chronic
infection and excessive inflammation - two fundamental factors of CFâs
physiopathology.
Inflammation plays a key role in the evolution of the illness and despite many
studies on this subject, the regulation of the inflammatory process remains a
mystery and CFTRâs role is not well established. Additionally, since the
physiopathology cannot be explained by mutation alone, several authors
suggest the importance of other factors (genetic and/or environmental) which
are factors in the clinical picture of the illness.
In our study, we use microarray technology to evaluate the transcriptional state
of an epithelial lung cell issued from a human with cystic fibrosis. Initially, our
analysis identifies 128 inflammatory genes which are over-expressed in the
cystic fibrosis cells versus non-cystic fibrosis cells, showing several
inflammatory gene families such as cytokines or calgranulins. An analysis of the
publications and annotations of these transcripts suggests that their
modulations depend upon the cascade of NF-ÎșB and/or signalling pathways associated with interferons (IFN). In other words, their modulations could be
associated with epigenetic modifications of their chromosomal loci. Secondly,
we study the transcriptional activity of an epithelial lung cell issued from a
human with cystic fibrosis in the presence of DMNQ, a cytotoxic molecule. Our
goal is to identify the biological processus which are disturbed by the mutation
of the CFTR gene in the presence of oxidative stress.
Based on a canonical redundancy analysis, we identify 60 genes associated
with cell death and their modulation in our study explained by the combined
effect of mutation and oxidative stress. By measuring the activity of caspase
3/7, an effector of apoptosis (programmed cell death), we see that the cells
containing the mutation ÎF508 could present a problem with apoptosis. Our
transcriptomic data suggest that decreased activity of the MAPK cascade and
over-expression of anti-apoptotic genes would be a factor in apoptotic
imbalance
Optically-gated resonant emission in single quantum dots
We report on the resonant emission in coherently-driven single semiconductor
quantum dots. We demonstrate that an ultra-weak non-resonant laser acts as an
optical gate for the quantum dot resonant response. We show that the gate laser
suppresses Coulomb blockade at the origin of a resonant emission quenching, and
that the optically-gated quantum dots systematically behave as ideal two-level
systems in both regimes of coherent and incoherent resonant emission
Photoneutralization and slow capture of carriers in quantum dots probed by resonant excitation spectroscopy
International audienceWe investigate experimentally and theoretically the resonant emission of single InAs/GaAs quantum dots in a planar microcavity. Due to the presence of at least one residual charge in the quantum dots, the resonant excitation of the neutral exciton is blocked. The influence of the residual doping on the initial quantum dots charge state is analyzed, and the resonant emission quenching is interpreted as a Coulomb blockade effect. The use of an additional non-resonant laser in a specific low power regime leads to the carrier draining in quantum dots and allows an efficient optical gating of the exciton resonant emission. A detailed population evolution model, developed to describe the carrier draining and the optical gate effect, perfectly fits the experimental results in the steady state and dynamical regimes of the optical gate with a single set of parameters. We deduce that ultra-slow Auger- and phonon-assisted capture processes govern the carrier draining in quantum dots with relaxation times in the 1 - 100 microsecond range. We conclude that the optical gate acts as a very sensitive probe of the quantum dots population relaxation in an unprecedented slow-capture regime
Neustonic microplastic and zooplankton in the North Western Mediterranean Sea
Neustonic microplastic and zooplankton abundance was determined in the North Western Mediterranean Sea during a summer cruise between July 9th and August 6th 2010, with a break between July 22th and 25th due to a strong wind event.
Ninety percent of the 40 stations contained microplastic particles (size 0.3-5 mm) of various compositions: e.g., filaments, polystyrene, thin plastic films. An average concentration of 0.116 particles/mÂČ was observed. The highest abundances (> 0.36 particles/mÂČ) were observed in the shelf stations.
The neustonic plastic particles concentrations were 5 times higher before than after the strong wind event which increased the mixing and the vertical repartition of plastic particles in the upper layers of the water column. The values rise in the same order of magnitude than in the North Pacific Gyre. The average ratio between microplastics and mesozooplankton weights was 0.5 for the whole survey and might induce a potential confusion for zooplankton feeders.Peer reviewe
Establishment Failure in Biological Invasions: A Case History of Littorina littorea in California, USA
The early stages of biological invasions are rarely observed, but can provide significant insight into the invasion process as well as the influence vectors have on invasion success or failure.We characterized three newly discovered populations of an introduced gastropod, Littorina littorea (Linné, 1758), in California, USA, comparing them to potential source populations in native Europe and the North American East Coast, where the snail is also introduced. Demographic surveys were used to assess spatial distribution and sizes of the snail in San Francisco and Anaheim Bays, California. Mitochondrial DNA was sequenced and compared among these nascent populations, and various populations from the North American East Coast and Europe, to characterize the California populations and ascertain their likely source. Demographic and genetic data were considered together to deduce likely vectors for the California populations. We found that the three large California L. littorea populations contained only adult snails and had unexpectedly high genetic diversity rather than showing an extreme bottleneck as typically expected in recent introductions. Haplotype diversity in Californian populations was significantly reduced compared to European populations, but not compared to East Coast populations. Genetic analyses clearly suggested the East Coast as the source region for the California introductions.The California L. littorea populations were at an early, non-established phase of invasion with no evidence of recruitment. The live seafood trade is the most likely invasion vector for these populations, as it preferentially transports large numbers of adult L. littorea, matching the demographic structure of the introduced California L. littorea populations. Our results highlight continued operation of live seafood trade vectors and the influence of vectors on the demographic and genetic structure of the resulting populations, especially early stages of the invasion process
Dissection of the Complex Phenotype in Cuticular Mutants of Arabidopsis Reveals a Role of SERRATE as a Mediator
Mutations in LACERATA (LCR), FIDDLEHEAD (FDH), and BODYGUARD (BDG) cause a complex developmental syndrome that is consistent with an important role for these Arabidopsis genes in cuticle biogenesis. The genesis of their pleiotropic phenotypes is, however, poorly understood. We provide evidence that neither distorted depositions of cutin, nor deficiencies in the chemical composition of cuticular lipids, account for these features, instead suggesting that the mutants alleviate the functional disorder of the cuticle by reinforcing their defenses. To better understand how plants adapt to these mutations, we performed a genome-wide gene expression analysis. We found that apparent compensatory transcriptional responses in these mutants involve the induction of wax, cutin, cell wall, and defense genes. To gain greater insight into the mechanism by which cuticular mutations trigger this response in the plants, we performed an overlap meta-analysis, which is termed MASTA (MicroArray overlap Search Tool and Analysis), of differentially expressed genes. This suggested that different cell integrity pathways are recruited in cesA cellulose synthase and cuticular mutants. Using MASTA for an in silico suppressor/enhancer screen, we identified SERRATE (SE), which encodes a protein of RNAâprocessing multi-protein complexes, as a likely enhancer. In confirmation of this notion, the se lcr and se bdg double mutants eradicate severe leaf deformations as well as the organ fusions that are typical of lcr and bdg and other cuticular mutants. Also, lcr does not confer resistance to Botrytis cinerea in a se mutant background. We propose that there is a role for SERRATE-mediated RNA signaling in the cuticle integrity pathway
Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling.
Neutrophils provide first line of host defense against bacterial infections utilizing glycolysis for their effector functions. How glycolysis and its major byproduct lactate are triggered in bone marrow (BM) neutrophils and their contribution to neutrophil mobilization in acute inflammation is not clear. Here we report that bacterial lipopolysaccharides (LPS) or Salmonella Typhimurium triggers lactate release by increasing glycolysis, NADPH-oxidase-mediated reactive oxygen species and HIF-1α levels in BM neutrophils. Increased release of BM lactate preferentially promotes neutrophil mobilization by reducing endothelial VE-Cadherin expression, increasing BM vascular permeability via endothelial lactate-receptor GPR81 signaling. GPR81-/- mice mobilize reduced levels of neutrophils in response to LPS, unless rescued by VE-Cadherin disrupting antibodies. Lactate administration also induces release of the BM neutrophil mobilizers G-CSF, CXCL1 and CXCL2, indicating that this metabolite drives neutrophil mobilization via multiple pathways. Our study reveals a metabolic crosstalk between lactate-producing neutrophils and BM endothelium, which controls neutrophil mobilization under bacterial infection
Detection chain and electronic readout of the QUBIC instrument
The Q and U Bolometric Interferometer for Cosmology (QUBIC) Technical Demonstrator (TD) aiming to shows the feasibility of the combination of interferometry and bolometric detection. The electronic readout system is based on an array of 128 NbSi Transition Edge Sensors cooled at 350mK readout with 128 SQUIDs at 1K controlled and amplified by an Application Specific Integrated Circuit at 40K. This readout design allows a 128:1 Time Domain Multiplexing. We report the design and the performance of the detection chain in this paper. The technological demonstrator unwent a campaign of test in the lab. Evaluation of the QUBIC bolometers and readout electronics includes the measurement of I-V curves, time constant and the Noise Equivalent Power. Currently the mean Noise Equivalent Power is ~ 2 x 10â»ÂčⶠW/âHz
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