Multimodal Social Book Search

International audienceToday's information retrieval applications have become increasingly complex. The Social Book Search (SBS) lab at CLEF 2015 allows evaluating retrieval methods on a complex search task with several textual and non-textual meta-data fields. The challenge is to incorporate the different information types (modalities) into a single ranked list. We build a strong textual baseline and combine it with a document prior based on social signals. Further, we include non-textual modalities in relation to the user preferences using random forest learning to rank. Our experiments show that both the social document prior and the learning to rank approach improve the search results

Requalification des logements de l'université polaire à Longyearbyen (Spitzberg, Région de Svalbard, Norvège)

Le site d'intervention se trouve à Longyearbyen sur l'île du Spitzberg, à moins de 1000 km du Pôle Nord, au-delà de la Norvège. Sa situation géographie éloignée, son climat rude, son accessibilité difficile due à la présence de la glace imposent d'importantes contraintes sur la construction. L'écologie et les réductions de pertes d'énergie sont des thèmes à ne pas négliger pour toute transformation ou nouvelle construction. La récupération et réutilisation de matériaux sont à considérer dans ce lieu où tout doit être importé. Actuellement, la ville ne connaît aucun lieu de rencontre, c'est pourquoi il est important de développer un site favorisant l'activité sociale et le partage culturel. Le projet propose la relocalisation des anciens logements de mineurs, actuellement trop éloignés du centre-ville, pour les réaffecter en lieux publics et en logements pour étudiants, professeurs et hôtes touristiques. Il favorise la création d'un vrai esprit de quartier dialoguant avec la nouvelle université polaire, la ville et la nature qui l'entourent

Blocking Junctional Adhesion Molecule C Enhances Dendritic Cell Migration and Boosts the Immune Responses against Leishmania major

The recruitment of dendritic cells to sites of infections and their migration to lymph nodes is fundamental for antigen processing and presentation to T cells. In the present study, we showed that antibody blockade of junctional adhesion molecule C (JAM-C) on endothelial cells removed JAM-C away from junctions and increased vascular permeability after L. major infection. This has multiple consequences on the output of the immune response. In resistant C57BL/6 and susceptible BALB/c mice, we found higher numbers of innate immune cells migrating from blood to the site of infection. The subsequent migration of dendritic cells (DCs) from the skin to the draining lymph node was also improved, thereby boosting the induction of the adaptive immune response. In C57BL/6 mice, JAM-C blockade after L. major injection led to an enhanced IFN-γ dominated T helper 1 (Th1) response with reduced skin lesions and parasite burden. Conversely, anti JAM-C treatment increased the IL-4-driven T helper 2 (Th2) response in BALB/c mice with disease exacerbation. Overall, our results show that JAM-C blockade can finely-tune the innate cell migration and accelerate the consequent immune response to L. major without changing the type of the T helper cell response

Blocking JAM-C increases the number of DCs migrating to the draining lymph node.

<p>(A) The ear draining lymph node cells were harvested and stained for FACS analysis 18 hours after FITC-painting. Representative FACS dot plots are shown. (B) The number of IA^high CD11c⁺ FITC⁺ migratory DCs was counted. Data are expressed as a percentage of the mean of the control group ± SEM of eighteen mice per group pooled from 3 separate experiments, and were analyzed by the unpaired Student's t test with ***: p<0.001. Raw data from one representative experiment are provided in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004550#ppat.1004550.s007" target="_blank">S7 Figure</a>.</p

Blocking JAM-C enhances DC migration and boosts the immune responses to <i>L. major</i> infection.

<p>By removing JAM-C out of functions, H33 increases adhesion of leukocytes and potentiates vascular permeability and cell migration of leukocytes after <i>L. major</i> infection. Increased numbers of recruited neutrophils result in higher levels of the chemokine CCL3 attracting monocytes and mo-DCs in C57BL/6 mice. The number of migratory DCs to lymph nodes increases, and the subsequent T cell response is mounted more efficiently. Resistant C57BL/6 mice develop a higher IFN-γ-dominated Th1 response while susceptible BALB/c mice develop a stronger IL-4-dominated Th2 response. This has a significant healing effect in resistant animals whereas susceptible mice display an exacerbated disease.</p

Blocking JAM-C boosts the Th2 cell response and worsens the disease in BALB/c mice.

<p>The number of emigrating neutrophils (A), mo-DCs (B), dermal DCs (C) and dermal mφ (D) was measured in the ears of H33-treated (H33, black bar) versus isotype control-treated mice (Ctr, white bars) 24 hours post <i>L. major</i> infection. Data represent the mean ± SEM of twelve mice per group pooled from 2 separate experiments, and were analyzed by the unpaired Student's t test with *: p<0.05. (E) Mice were inoculated with 2×10⁶ stationary phase <i>L. major</i> promastigotes in the ear dermis and treated with H33 or control antibody for 3 weeks. The area of the lesion was monitored weekly for 6 weeks. Representative ear pictures are shown. Scale bars, 1 mm. Data represent the mean ± SEM of twenty mice per group pooled from two separate experiments. (F–L) Mice were inoculated with 1×10⁴ stationary phase <i>L. major</i> promastigotes in the ear dermis and treated with H33 or control antibody for 3 weeks. The area of the lesion was monitored weekly for 4 weeks. Representative ear pictures are shown. Scale bars, 0.5 mm. Data represent the mean ± SEM of ten mice per group pooled from two separate experiments. (G–H) The parasite burden in infected ears (G) and draining lymph nodes (H) were measured by LDA. Data are expressed as a percentage of the mean of the control group ± SEM of mice from panel F. (I–J) The number of CD4⁺ (I) and CD8⁺ (J) T cells were measured. Data represent the mean ± SEM of mice from panel F. (K–L) Draining lymph nodes cells were restimulated with UV-irradiated <i>L. major</i> for 72 hours, and the IL-4 (K) and IFN-γ (L) produced were measured. Data are expressed as a percentage of the mean of the control group ± SEM of mice from panel F. Data were analyzed by the unpaired Student's t test with *:p<0.05 and **: p<0.01. For panels expressing results as a percentage of the mean of the control, raw data of one experiment are provided in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004550#ppat.1004550.s009" target="_blank">S9 Figure</a>.</p

The antibody H33 mimics JAM-C downregulation after L. major inoculation, and locally increases vascular permeability after infection.

<p>(A) JAM-C levels in endothelial cells populations of mouse ear. Ears were enzymatically digested and stained for FACS analysis. CD45⁻ CD31⁺ gp38⁻ cells represent blood endothelial cells (BECs), whereas CD45⁻ CD31⁺ gp38⁺ cells are lymphatic endothelial cells (LECs). For each population, a representative histogram overlay is shown with JAM-C in endothelial cells from naïve ears (black filled), JAM-C in endothelials cells from <i>L. major</i> infected ears (blank filled), and the isotype control staining (grey filled). (B) The median fluorescence intensity (MFI) of JAM-C in naïve mouse ears (white bars) versus <i>L. major</i> infected mouse ears (black bars) was measured in BECs and LECs. The Y-axis scale represents MFI normalized to the mean MFI of naïve ears. Data represent the mean ± SEM of ten individual mice pooled from two separate experiments, and were analyzed by the unpaired Student's t test with ***: p<0.001. (C) Mice were treated with H33 or control antibody 2 hours before Evans blue was injected i.v. and <i>L. major</i> inoculated i.d. in the ear dermis. Skin permeability was assessed by the absorbance of Evans blue extracted from the sample normalized to the weight of ear. Results are shown for naïve versus <i>L. major</i> infected animals treated with H33 (black bars) or control antibody (blank bars). Representative ear pictures are shown. Data represent the mean ± SEM of seventeen mice per group pooled from two separate experiments, and were analyzed by the unpaired Student's t test with ***: p<0.001. (D) Ear sections from control antibody-treated (top panel) or H33-treated mice (bottom panel) were stained for JAM-C (green) and CD31 (red). Nucleus was stained with DAPI (blue). Scale bars, 10 µm. Control staining for JAM-C is shown in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004550#ppat.1004550.s003" target="_blank">Figure S3</a>. (E) The pixel intensity across 10 representative cells of similar size taken from three mice per group was measured and expressed as a percentage of the maximal pixel intensity. Data represent the average profile plot for the 10 cells per group analyzed.</p

Blocking JAM-C improves the Th1 cell response and favours healing in C57BL/6 mice.

<p>(<b>A–E</b>) <b>Mice were inoculated with L. major in the ear dermis and treated with H33 or isotype control antibody for 3 weeks, twice a week.</b> (A) The area of the lesion was monitored weekly and representative pictures of ear lesions are shown at 4 and 8 weeks p.i. Scale bars, 0.5 mm. Data represent the mean ± SEM of twenty mice per group pooled from two separate experiments for the time point 4 weeks; and fifteen mice per group pooled from two separate experiments for the time point 8 weeks. (B) The parasite burden in infected ears was measured by LDA 4 and 8 weeks p.i. Data are expressed as a percentage of the mean of the control group ± SEM of mice from panel A. (C–D) The number of draining lymph node CD4⁺ (C) and CD8⁺ (D) T cells analyzed by flow cytometry 4 and 8 weeks p.i. Data represent the mean ± SEM of mice from panel A. (E) Draining lymph node cells were restimulated for 72 hrs with UV-irradiated <i>L. major</i> and the secreted IFN-γ was measured. Data are expressed as a percentage of the mean of the control group ± SEM of mice from panel A. Data were analyzed by the unpaired Student's t test with *:p<0.05 and **: p<0.01. For panels B and E, raw data from one experiment are also provided in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004550#ppat.1004550.s008" target="_blank">S8 Figure</a>.</p

Blocking JAM-C increases the number of leukocytes recruited to the site of <i>L. major</i> infection.

<p>(A) Representative dot plots of neutrophils (CD11b⁺ Ly6C⁺ Ly6G⁺); monocytes (CD11b⁺ Ly6C⁺ Ly6G⁻ CD11c⁻ IA⁻); mo-DCs (CD11b⁺ Ly6C⁺ Ly6G⁻ CD11c⁺ IA⁺); dermal mφ (CD11b⁺ Ly6C⁻ Ly6G⁻ CD11c^low IA⁺); dermal DCs (CD11b⁺ Ly6C⁻ Ly6G⁻ CD11c^high IA⁺) in control versus H33-treated animals. (B–F) The number of neutrophils (B), monocytes (C), mo-DCs (D), dermal mφ (E) and dermal DCs (F) was measured in the H33-treated (H33, black bar) versus isotype control-treated mice (Ctr, white bars) 24 hours p.i. Data represent the mean ± SEM of twenty mice per group pooled from 3 separate experiments, and were analyzed by the unpaired Student's t test with *: p<0.05 and **: p<0.01. (G) CCL3 protein levels normalized to the weight of ears were measured in H33-treated (H33, black bar) versus isotype control-treated mice (Ctr, white bars) 8 and 24 hours p.i. Data represent the mean ± SEM of ten mice per group pooled from 2 separate experiments, and were analyzed by the unpaired Student's t test with **: p<0.01. (H–I) The parasite burden in infected ears (H) and draining lymph nodes (LN) (I) were measured 48 hours p.i. by limiting dilution assay (LDA). Data are expressed as a percentage of the mean of the control group ± SEM of ten mice per group pooled from 2 separate experiments, and were analyzed by the unpaired Student's t test. For panel H and I, raw data of one representative experiment are provided in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004550#ppat.1004550.s006" target="_blank">S6 Figure</a>.</p

ILC Reference Design Report Volume 4 - Detectors

This report, Volume IV of the International Linear Collider Reference Design Report, describes the detectors which will record and measure the charged and neutral particles produced in the ILC's high energy e+e- collisions. The physics of the ILC, and the environment of the machine-detector interface, pose new challenges for detector design. Several conceptual designs for the detector promise the needed performance, and ongoing detector R&D is addressing the outstanding technological issues. Two such detectors, operating in push-pull mode, perfectly instrument the ILC interaction region, and access the full potential of ILC physics.This report, Volume IV of the International Linear Collider Reference Design Report, describes the detectors which will record and measure the charged and neutral particles produced in the ILC's high energy e+e- collisions. The physics of the ILC, and the environment of the machine-detector interface, pose new challenges for detector design. Several conceptual designs for the detector promise the needed performance, and ongoing detector R&D is addressing the outstanding technological issues. Two such detectors, operating in push-pull mode, perfectly instrument the ILC interaction region, and access the full potential of ILC physics