Etude exploratoire du stylo électronique pour le contrôle aérien

International audienceCurrent environment used by air traffic controllers mixes digital visualizations (radar screen), and tangible systems with paper strip. Despite the fact that paper strip are robust, flexible and complementary to the radar screen, authorities decided to abandon it in the profit of digital strip. The main issue of paper strip is that the system does not have access to the information written on it. In this paper, we studied an alternative solution with hybrids Anoto pens with contiuous streaming. We first retrieved important tasks performed by air traffic controller, second, we investigated to find out efficient interaction paradigm for their activity. Finally, we developed and assessed an operational prototype with new functionalities. This suggests that it is possible to retain advantages of existing paper strip while informing informatics systems and improving interaction

Supporting users tasks with personal information management and web forms augmentation

Currently, many tasks performed on the Web prompt users to provide personal information through forms. Despite the fact that most users are familiarized with this kind of interaction technique, the use of Web forms is not always straightforward. Indeed, some users might need assistance to understand labels and complex data format required to fill in form fields that, quite often, vary from a Web site to another even when requesting similar data. Filling in forms can be tedious and repetitive as many Web sites request similar information. In this work we analyze user's interactions with Web forms and propose an approach for enhancing Web forms using client-side adaptation techniques in order to assist users to fill in Web forms. As the use of Web forms is closely related to the management of personal information our approach includes the support for data exchange between user's personal information management systems (PIMs) and third-party Web forms. The approach is illustrated by a set of client-side adaptation tools and a pervasive Personal Information Management Systems called PIMI.Publicado en Lecture Notes in Computer Science book series (vol. 7387).Laboratorio de Investigación y Formación en Informática Avanzad

Supporting users tasks with personal information management and web forms augmentation

Currently, many tasks performed on the Web prompt users to provide personal information through forms. Despite the fact that most users are familiarized with this kind of interaction technique, the use of Web forms is not always straightforward. Indeed, some users might need assistance to understand labels and complex data format required to fill in form fields that, quite often, vary from a Web site to another even when requesting similar data. Filling in forms can be tedious and repetitive as many Web sites request similar information. In this work we analyze user's interactions with Web forms and propose an approach for enhancing Web forms using client-side adaptation techniques in order to assist users to fill in Web forms. As the use of Web forms is closely related to the management of personal information our approach includes the support for data exchange between user's personal information management systems (PIMs) and third-party Web forms. The approach is illustrated by a set of client-side adaptation tools and a pervasive Personal Information Management Systems called PIMI.Publicado en Lecture Notes in Computer Science book series (vol. 7387).Laboratorio de Investigación y Formación en Informática Avanzad

The p.Arg63Trp polymorphism controls Vav1 functions and Foxp3 regulatory T cell development

A single nucleotide polymorphism causing constitutive activation of Vav1 results in increased natural Treg generation and is responsible for the imbalance between Vav1 GEF and adaptor functions

E-Cadherin–dependent Growth Suppression is Mediated by the Cyclin-dependent Kinase Inhibitor p27KIP1

Recent studies have demonstrated the importance of E-cadherin, a homophilic cell–cell adhesion molecule, in contact inhibition of growth of normal epithelial cells. Many tumor cells also maintain strong intercellular adhesion, and are growth-inhibited by cell– cell contact, especially when grown in three-dimensional culture. To determine if E-cadherin could mediate contact-dependent growth inhibition of nonadherent EMT/6 mouse mammary carcinoma cells that lack E-cadherin, we transfected these cells with an exogenous E-cadherin expression vector. E-cadherin expression in EMT/6 cells resulted in tighter adhesion of multicellular spheroids and a reduced proliferative fraction in three-dimensional culture. In addition to increased cell–cell adhesion, E-cadherin expression also resulted in dephosphorylation of the retinoblastoma protein, an increase in the level of the cyclin-dependent kinase inhibitor p27kip1 and a late reduction in cyclin D1 protein. Tightly adherent spheroids also showed increased levels of p27 bound to the cyclin E-cdk2 complex, and a reduction in cyclin E-cdk2 activity. Exposure to E-cadherin–neutralizing antibodies in three-dimensional culture simultaneously prevented adhesion and stimulated proliferation of E-cadherin transfectants as well as a panel of human colon, breast, and lung carcinoma cell lines that express functional E-cadherin. To test the importance of p27 in E-cadherin–dependent growth inhibition, we engineered E-cadherin–positive cells to express inducible p27. By forcing expression of p27 levels similar to those observed in aggregated cells, the stimulatory effect of E-cadherin–neutralizing antibodies on proliferation could be inhibited. This study demonstrates that E-cadherin, classically described as an invasion suppressor, is also a major growth suppressor, and its ability to inhibit proliferation involves upregulation of the cyclin-dependent kinase inhibitor p27

The Fission Yeast Stress-Responsive MAPK Pathway Promotes Meiosis via the Phosphorylation of Pol II CTD in Response to Environmental and Feedback Cues

The RRM-type RNA-binding protein Mei2 is a master regulator of meiosis in fission yeast, in which it stabilizes meiosis-specific mRNAs by blocking their destruction. Artificial activation of Mei2 can provoke the entire meiotic process, and it is suspected that Mei2 may do more than the stabilization of meiosis-specific mRNAs. In our current study using a new screening system, we show that Mei2 genetically interacts with subunits of CTDK-I, which phosphorylates serine-2 residues on the C-terminal domain of RNA polymerase II (Pol II CTD). Phosphorylation of CTD Ser-2 is essential to enable the robust transcription of ste11, which encodes an HMG-type transcription factor that regulates the expression of mei2 and other genes necessary for sexual development. CTD Ser-2 phosphorylation increases under nitrogen starvation, and the stress-responsive MAP kinase pathway, mediated by Wis1 MAPKK and Sty1 MAPK, is critical for this stress response. Sty1 phosphorylates Lsk1, the catalytic subunit of CTDK-I. Furthermore, a feedback loop stemming from activated Mei2 to Win1 and Wis4 MAPKKKs operates in this pathway and eventually enhances CTD Ser-2 phosphorylation and ste11 transcription. Hence, in addition to starting meiosis, Mei2 functions to reinforce the commitment to it, once cells have entered this process. This study also demonstrates clearly that the stress-responsive MAP kinase pathway can modulates gene expression through phosphorylation of Pol II CTD

Phosphorylation-Independent Regulation of Atf1-Promoted Meiotic Recombination by Stress-Activated, p38 Kinase Spc1 of Fission Yeast

BACKGROUND:Stress-activated protein kinases regulate multiple cellular responses to a wide variety of intracellular and extracellular conditions. The conserved, multifunctional, ATF/CREB protein Atf1 (Mts1, Gad7) of fission yeast binds to CRE-like (M26) DNA sites. Atf1 is phosphorylated by the conserved, p38-family kinase Spc1 (Sty1, Phh1) and is required for many Spc1-dependent stress responses, efficient sexual differentiation, and activation of Rec12 (Spo11)-dependent meiotic recombination hotspots like ade6-M26. METHODOLOGY/PRINCIPAL FINDINGS:We sought to define mechanisms by which Spc1 regulates Atf1 function at the ade6-M26 hotspot. The Spc1 kinase was essential for hotspot activity, but dispensable for basal recombination. Unexpectedly, a protein lacking all eleven MAPK phospho-acceptor sites and detectable phosphorylation (Atf1-11M) was fully proficient for hotspot recombination. Furthermore, tethering of Atf1 to ade6 in the chromosome by a heterologous DNA binding domain bypassed the requirement for Spc1 in promoting recombination. CONCLUSIONS/SIGNIFICANCE:The Spc1 protein kinase regulates the pathway of Atf1-promoted recombination at or before the point where Atf1 binds to chromosomes, and this pathway regulation is independent of the phosphorylation status of Atf1. Since basal recombination is Spc1-independent, the principal function of the Spc1 kinase in meiotic recombination is to correctly position Atf1-promoted recombination at hotspots along chromosomes. We also propose new hypotheses on regulatory mechanisms for shared (e.g., DNA binding) and distinct (e.g., osmoregulatory vs. recombinogenic) activities of multifunctional, stress-activated protein Atf1

Genomic Binding Profiling of the Fission Yeast Stress-Activated MAPK Sty1 and the bZIP Transcriptional Activator Atf1 in Response to H2O2

10.1371/journal.pone.0011620PLoS ONE57