Université de Sherbrooke

About: Université de Sherbrooke is a education organization based out in Sherbrooke, Quebec, Canada. It is known for research contribution in the topics: Population & Receptor. The organization has 14922 authors who have published 28783 publications receiving 792511 citations. The organization is also known as: Universite de Sherbrooke & Sherbrooke University.

Mobile Robotic Toys and Autism

Abstract: To help children with autism develop social skills, we are investigating the use of mobile robotic toys that can move autonomously in the environment and interact in various manners (vocal messages, music, visual cues, movement, etc.),in a more predictable and less intimidating way. These interactions are designed to build up their self-esteem by reinforcing what they do well. We report tests done with autistic children using different robots, each robot having particular characteristics that allow to create interesting interactions with each child.

Differential β-Arrestin–Dependent Conformational Signaling and Cellular Responses Revealed by Angiotensin Analogs

Abstract: The angiotensin type 1 receptor (AT1R) and its octapeptide ligand, angiotensin II (AngII), engage multiple downstream signaling pathways, including those mediated by heterotrimeric guanosine triphosphate-binding proteins (G proteins) and those mediated by β-arrestin. Here, we examined AT1R-mediated Gα(q) and β-arrestin signaling with multiple AngII analogs bearing substitutions at position 8, which is critical for binding to the AT1R and its activation of G proteins. Using assays that discriminated between ligand-promoted recruitment of β-arrestin to the AT1R and its resulting conformational rearrangement, we extend the concept of biased signaling to include the analog's propensity to differentially promote conformational changes in β-arrestin, two responses that were differentially affected by distinct G protein-coupled receptor kinases. The efficacy of AngII analogs in activating extracellular signal-regulated kinases 1 and 2 correlated with the stability of the complexes between β-arrestin and AT1R in endosomes, rather than with the extent of β-arrestin recruitment to the receptor. In vascular smooth muscle cells, the ligand-induced conformational changes in β-arrestin correlated with whether the ligand promoted β-arrestin-dependent migration or proliferation. Our data indicate that biased signaling not only occurs between G protein- and β-arrestin-mediated pathways but also occurred at the level of the AT1R and β-arrestin, such that different AngII analogs selectively engaged distinct β-arrestin conformations, which led to specific signaling events and cell responses.

Affect-LM: A Neural Language Model for Customizable Affective Text Generation

Abstract: Human verbal communication includes affective messages which are conveyed through use of emotionally colored words. There has been a lot of research effort in this direction but the problem of integrating state-of-the-art neural language models with affective information remains an area ripe for exploration. In this paper, we propose an extension to an LSTM (Long Short-Term Memory) language model for generation of conversational text, conditioned on affect categories. Our proposed model, Affect-LM enables us to customize the degree of emotional content in generated sentences through an additional design parameter. Perception studies conducted using Amazon Mechanical Turk show that Affect-LM can generate naturally looking emotional sentences without sacrificing grammatical correctness. Affect-LM also learns affect-discriminative word representations, and perplexity experiments show that additional affective information in conversational text can improve language model prediction.

Clara cell protein (CC-16) induces a phospholipase A2-mediated inhibition of fibroblast migration in vitro.

Abstract: Clara cell protein (CC-16, also designated CC-10) is synthesized by the bronchiolar epithelium and has been suggested as an inhibitor of phospholipase A(2) (PLA(2)) activity. Therefore, CC-16 is a candidate for controlling inflammatory events in the lung. Because CC-16 amounts and function may be altered in fibrosing lung diseases in which bronchiolar injury has been reported, it was measured in alveolar fluids and sera. Secretory PLA(2) activity in alveolar fluids and the influence of CC-16 on platelet-derived growth factor-induced human fibroblast chemotaxis and cytosolic PLA(2) activity were also explored. CC-16 content was decreased in alveolar fluids from idiopathic pulmonary fibrosis (IPF: 1.3 +/- 0.1 mg/L) and bleomycin lung (1.1 +/- 0.2 versus 2.1 +/- 0.2 mg/L in controls, p < 0.05), whereas there was a three- to ninefold increase in secretory PLA(2) activity (p < 0.05 versus controls). CC-16 inhibited fibroblast chemotaxis in a dose-dependent manner (90% inhibition at 30 mu g/ml CC-16). This inhibition was reversed by reducing CC-16. CC-16 was also able to lower fibroblastic cytosolic PLA(2) activity by 50% in vitro. In summary, CC-16 is able to inhibit fibroblast chemotaxis in vitro by mechanisms that may be related to a blockage of cytosolic PLA(2) activity. It can be postulated that CC-16 deficiency may contribute to fibroblast burden activity in fibrosing lung diseases.