Solar wind turbulent spectrum at plasma kinetic scales

The description of the turbulent spectrum of magnetic fluctuations in the solar wind in the kinetic range of scales is not yet completely established. Here, we perform a statistical study of 100 spectra measured by the STAFF instrument on the Cluster mission, which allows to resolve turbulent fluctuations from ion scales down to a fraction of electron scales, i.e. from $\sim 10^2$ km to $\sim 300$ m. We show that for $k_{\perp}\rho_e \in[0.03,3]$ (that corresponds approximately to the frequency in the spacecraft frame $f\in [3,300]$ Hz), all the observed spectra can be described by a general law $E(k_\perp)\propto k_\perp^{-8/3}\exp{(-k_\perp \rho_e)}$, where $k_{\perp}$ is the wave-vector component normal to the background magnetic field and $\rho_e$ the electron Larmor radius. This exponential tail found in the solar wind seems compatible with the Landau damping of magnetic fluctuations onto electrons.Comment: published in APJ, 15 of November 2012 (with reduced "Discussion" section

Spectra and anisotropy of magnetic fluctuations in the Earth's magnetosheath: Cluster observations

We investigate the spectral shape, the anisotropy of the wave vector distributions and the anisotropy of the amplitudes of the magnetic fluctuations in the Earth's magnetosheath within a broad range of frequencies. We present the first observations of a Kolmogorov-like inertial range of Alfvenic fluctuations in the magnetosheath flanks, below fci. In the vicinity of fci, a spectral break is observed, like in solar wind turbulence. Above the break, the energy of compressive and Alfvenic fluctuations generally follow a power law with a spectral index between -3 and -2. Concerning the anisotropy of the wave vector distribution, we observe a change in its nature in the vicinity of ion characteristic scales: if at MHD scales there is no evidence for a dominance of a slab (k||>kperp) or 2D (kperp>k||) turbulence, above the spectral break, (f>fci, kc/wpi>1) the 2D turbulence dominates. This 2D turbulence is observed in six selected one-hour intervals among which the average proton beta varies from 0.8 to 9. It is observed for both the transverse and compressive magnetic fluctuations, independently on the presence of linearly unstable modes at low frequencies or Alfven vortices at the spectral break. We then analyse the anisotropy of the magnetic fluctuations in a time dependent reference frame based on the field B and the flow velocity V directions. Within the range of the 2D turbulence, at scales [1,30]kc/wpi, and for any beta we find that the magnetic fluctuations at a given frequency in the plane perpendicular to B have more energy along the BxV direction. This non-gyrotropy of the fluctuations is consistent with gyrotropic fluctuations at a given wave vector, with kperp>k||, which suffer a different Doppler shift along and perpendicular to V in the plane perpendicular to B.Comment: accepted for publication in Annales Geophysicae (ANGEO) at 29/09/200

PAX2 is activated by estradiol in breast cancer cells of the luminal subgroup selectively, to confer a low invasive phenotype

<p>Abstract</p> <p>Background</p> <p>Metastasis is the leading cause of death among breast cancer patients. Identifying key cellular factors controlling invasion and metastasis of breast cancer cells should pave the way to new therapeutic strategies efficiently interfering with the metastatic process. PAX2 (paired box 2) transcription factor is expressed by breast cancer cells <it>in vivo </it>and recently, it was shown to negatively regulate the expression of ERBB2 (erythroblastic leukemia viral oncogene homolog 2, HER-2/neu), a well-documented pro-invasive and pro-metastastic gene, in luminal/ERalpha-positive (ERα+) breast cancer cells. The objective of the present study was to investigate a putative role for PAX2 in the control of luminal breast cancer cells invasion, and to begin to characterize its regulation.</p> <p>Results</p> <p>PAX2 activity was higher in cell lines from luminal compared to non-luminal subtype, and activation of PAX2 by estradiol was selectively achieved in breast cancer cell lines of the luminal subtype. This process was blocked by ICI 182780 and could be antagonized by IGF-1. Knockdown of PAX2 in luminal MCF-7 cells completely abrogated estradiol-induced downregulation of ERBB2 and decrease of cell invasion, whereas overexpression of PAX2 in these cells enhanced estradiol effects on ERBB2 levels and cell invasion.</p> <p>Conclusions</p> <p>The study demonstrates that PAX2 activation by estradiol is selectively achieved in breast cancer cells of the luminal subtype, via ERα, and identifies IGF-1 as a negative regulator of PAX2 activity in these cells. Further, it reveals a new role for PAX2 in the maintenance of a low invasive behavior in luminal breast cancer cells upon exposure to estradiol, and shows that overexpression and activation of PAX2 in these cells is sufficient to reduce their invasive ability.</p

Toll-like receptor and pro-inflammatory cytokine expression during prolonged hyperinsulinaemia in horses: Implications for laminitis

Equine laminitis, a disease of the lamellar structure of the horse’s hoof, can be incited by numerous factors that include inflammatory and metabolic aetiologies. However, the role of inflammation in hyperinsulinaemic laminitis has not been adequately defined. Tolllike receptor (TLR) activation results in up-regulation of inflammatory pathways and the release of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-�), and may be a pathogenic factor in laminitis. The aim of this study was to determine whether TLR4 expression and subsequent pro-inflammatory cytokine production is increased in lamellae and skeletal muscle during equine hyperinsulinaemia. Standardbred horses were treated with either a prolonged, euglycaemic hyperinsulinaemic clamp (p-EHC) or a prolonged, glucose infusion (p-GI), which induced marked and moderate hyperinsulinaemia, respectively. Age-matched control horses were treated simultaneously with a balanced electrolyte solution. Treated horses developed clinical (p-EHC) or subclinical (p-GI) laminitis, whereas controls did not. Skeletal muscle and lamellar protein extracts were analysed by Western blotting for TLR4, IL-6, TNF-� and suppressor of cytokine signalling 3 (SOCS3) expression. Lamellar protein expression of TLR4 and TNF-�, but not IL-6, was increased by the p-EHC, compared to control horses. A significant positive correlation was found between lamellar TLR4 and SOCS3. Skeletal muscle protein expression of TLR4 signalling parameters did not differ between control and p-EHC-treated horses. Similarly, the p-GI did not result in up-regulation of lamellar protein expression of any parameter. The results suggest that insulin-sensitive tissues may not accurately reflect lamellar pathology during hyperinsulinaemia. While TLR4 is present in the lamellae, its activation appears unlikely to contribute significantly to the developmental pathogenesis of hyperinsulinaemic laminitis. However, inflammation may have a role to play in the later stages (e.g., repair or remodelling) of the disease

Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat

International audienceThis study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects