Combinatorics of BB-orbits and Bruhat--Chevalley order on involutions

Let $B$ be the group of invertible upper-triangular complex $n\times n$ matrices, $\mathfrak{u}$ the space of upper-triangular complex matrices with zeroes on the diagonal and $\mathfrak{u}^*$ its dual space. The group $B$ acts on $\mathfrak{u}^*$ by $(g.f)(x)=f(gxg^{-1})$, $g\in B$, $f\in\mathfrak{u}^*$, $x\in\mathfrak{u}$. To each involution $\sigma$ in $S_n$, the symmetric group on $n$ letters, one can assign the $B$-orbit $\Omega_{\sigma}\in\mathfrak{u}^*$. We present a combinatorial description of the partial order on the set of involutions induced by the orbit closures. The answer is given in terms of rook placements and is dual to A. Melnikov's results on $B$-orbits on $\mathfrak{u}$. Using results of F. Incitti, we also prove that this partial order coincides with the restriction of the Bruhat--Chevalley order to the set of involutions.Comment: 27 page

The Herschel view of the on-going star formation in the Vela-C molecular cloud

As part of the Herschel guaranteed time key program 'HOBYS', we present the photometric survey of the star forming region Vela-C, one of the nearest sites of low-to-high-mass star formation in the Galactic plane. Vela-C has been observed with PACS and SPIRE in parallel mode between 70 um and 500 um over an area of about 3 square degrees. A photometric catalogue has been extracted from the detections in each band, using a threshold of 5 sigma over the local background. Out of this catalogue we have selected a robust sub-sample of 268 sources, of which 75% are cloud clumps and 25% are cores. Their Spectral Energy Distributions (SEDs) have been fitted with a modified black body function. We classify 48 sources as protostellar and 218 as starless. For two further sources, we do not provide a secure classification, but suggest they are Class 0 protostars. From SED fitting we have derived key physical parameters. Protostellar sources are in general warmer and more compact than starless sources. Both these evidences can be ascribed to the presence of an internal source(s) of moderate heating, which also causes a temperature gradient and hence a more peaked intensity distribution. Moreover, the reduced dimensions of protostellar sources may indicate that they will not fragment further. A virial analysis of the starless sources gives an upper limit of 90% for the sources gravitationally bound and therefore prestellar. We fit a power law N(logM) prop M^-1.1 to the linear portion of the mass distribution of prestellar sources. This is in between that typical of CO clumps and those of cores in nearby star-forming regions. We interpret this as a result of the inhomogeneity of our sample, which is composed of comparable fractions of clumps and cores.Comment: 9 pages, 7 figures, accepted by A&

Mass‐loading the Earth's dayside magnetopause boundary layer and its effect on magnetic reconnection

When the interplanetary magnetic field is northward for a period of time, O+ from the high‐latitude ionosphere escapes along reconnected magnetic field lines into the dayside magnetopause boundary layer. Dual‐lobe reconnection closes these field lines, which traps O+ and mass loads the boundary layer. This O+ is an additional source of magnetospheric plasma that interacts with magnetosheath plasma through magnetic reconnection. This mass loading and interaction is illustrated through analysis of a magnetopause crossing by the Magnetospheric Multiscale spacecraft. While in the O+‐rich boundary layer, the interplanetary magnetic field turns southward. As the Magnetospheric Multiscale spacecraft cross the high‐shear magnetopause, reconnection signatures are observed. While the reconnection rate is likely reduced by the mass loading, reconnection is not suppressed at the magnetopause. The high‐latitude dayside ionosphere is therefore a source of magnetospheric ions that contributes often to transient reduction in the reconnection rate at the dayside magnetopause.publishedVersio

Specific immunotherapy by the sublingual route for respiratory allergy

Specific immunotherapy is the only treatment able to act on the causes and not only on the symptoms of respiratory allergy. Sublingual immunotherapy (SLIT) was introduced as an option to subcutaneous immunotherapy (SCIT), the clinical effectiveness of which is partly counterbalanced by the issue of adverse systemic reactions, which occur at a frequency of about 0.2% of injections and 2-5% of the patients and may also be life-threatening. A large number of trials, globally evaluated by several meta-analyses, demonstrated that SLIT is an effective and safe treatment for allergic rhinitis and allergic asthma, severe reactions being extremely rare. The application of SLIT is favored by a good compliance, higher than that reported for SCIT, in which the injections are a major factor for noncompliance because of inconvenience, and by its cost-effectiveness. In fact, a number of studies showed that SLIT may be very beneficial to the healthcare system, especially when its effectiveness persists after treatment withdrawal because of the induced immunologic changes

TRPA1 Contributes to the Acute Inflammatory Response and Mediates Carrageenan-Induced Paw Edema in the Mouse

Transient receptor potential ankyrin 1 (TRPA1) is an ion channel involved in thermosensation and nociception. TRPA1 is activated by exogenous irritants and also by oxidants formed in inflammatory reactions. However, our understanding of its role in inflammation is limited. Here, we tested the hypothesis that TRPA1 is involved in acute inflammatory edema. The TRPA1 agonist allyl isothiocyanate (AITC) induced inflammatory edema when injected intraplantarly to mice, mimicking the classical response to carrageenan. Interestingly, the TRPA1 antagonist HC-030031 and the cyclo-oxygenase (COX) inhibitor ibuprofen inhibited not only AITC but also carrageenan-induced edema. TRPA1-deficient mice displayed attenuated responses to carrageenan and AITC. Furthermore, AITC enhanced COX-2 expression in HEK293 cells transfected with human TRPA1, a response that was reversed by HC-030031. This study demonstrates a hitherto unknown role of TRPA1 in carrageenan-induced inflammatory edema. The results also strongly suggest that TRPA1 contributes, in a COX-dependent manner, to the development of acute inflammation

CD47 plays a critical role in T-cell recruitment by regulation of LFA-1 and VLA-4 integrin adhesive functions

CD47 plays an important but incompletely understood role in the innate and adaptive immune responses. CD47, also called integrin-associated protein, has been demonstrated to associate in cis with β1 and β3 integrins. Here we test the hypothesis that CD47 regulates adhesive functions of T-cell α4β1 (VLA-4) and αLβ2 (LFA-1) in in vivo and in vitro models of inflammation. Intravital microscopy studies reveal that CD47(−/−) Th1 cells exhibit reduced interactions with wild-type (WT) inflamed cremaster muscle microvessels. Similarly, murine CD47(−/−) Th1 cells, as compared with WT, showed defects in adhesion and transmigration across tumor necrosis factor-α (TNF-α)–activated murine endothelium and in adhesion to immobilized intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion protein 1 (VCAM-1) under flow conditions. Human Jurkat T-cells lacking CD47 also showed reduced adhesion to TNF-α–activated endothelium and ICAM-1 and VCAM-1. In cis interactions between Jurkat T-cell β2 integrins and CD47 were detected by fluorescence lifetime imaging microscopy. Unexpectedly, Jurkat CD47 null cells exhibited a striking defect in β1 and β2 integrin activation in response to Mn(2+) or Mg(2+)/ethylene glycol tetraacetic acid treatment. Our results demonstrate that CD47 associates with β2 integrins and is necessary to induce high-affinity conformations of LFA-1 and VLA-4 that recognize their endothelial cell ligands and support leukocyte adhesion and transendothelial migration

Highly Pathogenic Avian Influenza Virus Subtype H5N1 in Africa: A Comprehensive Phylogenetic Analysis and Molecular Characterization of Isolates

Highly pathogenic avian influenza virus A/H5N1 was first officially reported in Africa in early 2006. Since the first outbreak in Nigeria, this virus spread rapidly to other African countries. From its emergence to early 2008, 11 African countries experienced A/H5N1 outbreaks in poultry and human cases were also reported in three of these countries. At present, little is known of the epidemiology and molecular evolution of A/H5N1 viruses in Africa. We have generated 494 full gene sequences from 67 African isolates and applied molecular analysis tools to a total of 1,152 A/H5N1 sequences obtained from viruses isolated in Africa, Europe and the Middle East between 2006 and early 2008. Detailed phylogenetic analyses of the 8 gene viral segments confirmed that 3 distinct sublineages were introduced, which have persisted and spread across the continent over this 2-year period. Additionally, our molecular epidemiological studies highlighted the association between genetic clustering and area of origin in a majority of cases. Molecular signatures unique to strains isolated in selected areas also gave us a clearer picture of the spread of A/H5N1 viruses across the continent. Mutations described as typical of human influenza viruses in the genes coding for internal proteins or associated with host adaptation and increased resistance to antiviral drugs have also been detected in the genes coding for transmembrane proteins. These findings raise concern for the possible human health risk presented by viruses with these genetic properties and highlight the need for increased efforts to monitor the evolution of A/H5N1 viruses across the African continent. They further stress how imperative it is to implement sustainable control strategies to improve animal and public health at a global level