Code and its image: the functions of text and visualisation in a code-based design studio

Traditionally, design learning in the architecture studio has taken place through a combination of individual work and joint projects. The introduction of code-based design practices in the design studio has altered this balance, introducing new models of joint authorship and new ways for individuals to contribute to co-authored projects. This paper presents a case study describing four design studios in a higher education setting that used code as a tool for generating architectural geometry. The format of the studios encouraged the students to reflect critically on their role as authors and to creatively address the multiple opportunities for shared authorship available with code-based production. The research question addressed in this study involved the role of code-based practices in altering the model of architectural education in the design studio, in particular the role of visual representations of a code-based design process in the production of shared knowledge

Une ambiance lumineuse en fonction des besoins

Presentation of the ECAL-EPFL collaborative project in user-robot swarm interaction

An immune-inspired swarm aggregation algorithm for self-healing swarm robotic systems

© 2016 Elsevier Ireland Ltd Swarm robotics is concerned with the decentralised coordination of multiple robots having only limited communication and interaction abilities. Although fault tolerance and robustness to individual robot failures have often been used to justify the use of swarm robotic systems, recent studies have shown that swarm robotic systems are susceptible to certain types of failure. In this paper we propose an approach to self-healing swarm robotic systems and take inspiration from the process of granuloma formation, a process of containment and repair found in the immune system. We use a case study of a swarm performing team work where previous works have demonstrated that partially failed robots have the most detrimental effect on overall swarm behaviour. We have developed an immune inspired approach that permits the recovery from certain failure modes during operation of the swarm, overcoming issues that effect swarm behaviour associated with partially failed robots

Modelling a wireless connected swarm of mobile robots

It is a characteristic of swarm robotics that modelling the overall swarm behaviour in terms of the low-level behaviours of individual robots is very difficult. Yet if swarm robotics is to make the transition from the laboratory to real-world engineering realisation such models would be critical for both overall validation of algorithm correctness and detailed parameter optimisation. We seek models with predictive power: models that allow us to determine the effect of modifying parameters in individual robots on the overall swarm behaviour. This paper presents results from a study to apply the probabilistic modelling approach to a class of wireless connected swarms operating in unbounded environments. The paper proposes a probabilistic finite state machine (PFSM) that describes the network connectivity and overall macroscopic behaviour of the swarm, then develops a novel robot-centric approach to the estimation of the state transition probabilities within the PFSM. Using measured data from simulation the paper then carefully validates the PFSM model step by step, allowing us to assess the accuracy and hence the utility of the model. © Springer Science + Business Media, LLC 2008

CD8 positive T cells express IL-17 in patients with chronic obstructive pulmonary disease

<p>Abstract</p> <p>Background</p> <p>Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory disease of the lung. The nature of the immune reaction in COPD raises the possibility that IL-17 and related cytokines may contribute to this disorder. This study analyzed the expression of IL-17A and IL-17F as well as the phenotype of cells producing them in bronchial biopsies from COPD patients.</p> <p>Methods</p> <p>Bronchoscopic biopsies of the airway were obtained from 16 COPD subjects (GOLD stage 1-4) and 15 control subjects. Paraffin sections were used for the investigation of IL-17A and IL-17F expression in the airways by immunohistochemistry, and frozen sections were used for the immunofluorescence double staining of IL-17A or IL-17F paired with CD4 or CD8. In order to confirm the expression of IL-17A and IL-17F at the mRNA level, a quantitative RT-PCR was performed on the total mRNA extracted from entire section or CD8 positive cells selected by laser capture microdissection.</p> <p>Results</p> <p>IL-17F immunoreactivity was significantly higher in the bronchial biopsies of COPD patients compared to control subjects (<it>P </it>< 0.0001). In the submucosa, the absolute number of both IL-17A and IL-17F positive cells was higher in COPD patients (<it>P </it>< 0.0001). After adjusting for the total number of cells in the submucosa, we still found that more cells were positive for both IL-17A (<it>P </it>< 0.0001) and IL-17F (<it>P </it>< 0.0001) in COPD patients compared to controls. The mRNA expression of IL-17A and IL-17F in airways of COPD patients was confirmed by RT-PCR. The expression of IL-17A and IL-17F was co-localized with not only CD4 but also CD8, which was further confirmed by RT-PCR on laser capture microdissection selected CD8 positive cells.</p> <p>Conclusion</p> <p>These findings support the notion that Th17 cytokines could play important roles in the pathogenesis of COPD, raising the possibility of using this mechanism as the basis for novel therapeutic approaches.</p

Downregulation of Integrin β4 Decreases the Ability of Airway Epithelial Cells to Present Antigens

Airway epithelial cells have been demonstrated to be accessory antigen presentation cells (APC) capable of activating T cells and may play an important role in the development of allergic airway inflammation of asthma. In asthmatic airways, loss of expression of the adhesion molecule integrin β4 (ITGB4) and an increase in Th2 inflammation bias has been observed in our previous study. Given that ITGB4 is engaged in multiple signaling pathways, we studied whether disruption of ITGB4-mediated cell adhesion may contribute to the adaptive immune response of epithelial cells, including their ability to present antigens, induce the activate and differentiate of T cells. We silenced ITGB4 expression in bronchial epithelial cells with an effective siRNA vector and studied the effects of ITGB4 silencing on the antigen presentation ability of airway epithelial cells. T cell proliferation and cytokine production was investigated after co-culturing with ITGB4-silenced epithelial cells. Surface expression of B7 homologs and the major histocompatibility complex (MHC) class II was also detected after ITGB4 was silenced. Our results demonstrated that silencing of ITGB4 resulted in impaired antigen presentation processes and suppressed T cell proliferation. Meanwhile, decrease in Th1 cytokine production and increase in Th17 cytokine production was induced after co-culturing with ITGB4-silenced epithelial cells. Moreover, HLA-DR was decreased and the B7 homologs expression was different after ITGB4 silencing. Overall, this study suggested that downregulation of ITGB4 expression in airway epithelial cells could impair the antigen presentation ability of these cells, which further regulate airway inflammation reaction in allergic asthma

LRRK2 protein levels are determined by kinase function and are crucial for kidney and lung homeostasis in mice

Mutations in leucine-rich repeat kinase 2 (LRRK2) cause late-onset Parkinson's disease (PD), but the underlying pathophysiological mechanisms and the normal function of this large multidomain protein remain speculative. To address the role of this protein in vivo, we generated three different LRRK2 mutant mouse lines. Mice completely lacking the LRRK2 protein (knock-out, KO) showed an early-onset (age 6 weeks) marked increase in number and size of secondary lysosomes in kidney proximal tubule cells and lamellar bodies in lung type II cells. Mice expressing a LRRK2 kinase-dead (KD) mutant from the endogenous locus displayed similar early-onset pathophysiological changes in kidney but not lung. KD mutants had dramatically reduced full-length LRRK2 protein levels in the kidney and this genetic effect was mimicked pharmacologically in wild-type mice treated with a LRRK2-selective kinase inhibitor. Knock-in (KI) mice expressing the G2019S PD-associated mutation that increases LRRK2 kinase activity showed none of the LRRK2 protein level and histopathological changes observed in KD and KO mice. The autophagy marker LC3 remained unchanged but kidney mTOR and TCS2 protein levels decreased in KD and increased in KO and KI mice. Unexpectedly, KO and KI mice suffered from diastolic hypertension opposed to normal blood pressure in KD mice. Our findings demonstrate a role for LRRK2 in kidney and lung physiology and further show that LRRK2 kinase function affects LRRK2 protein steady-state levels thereby altering putative scaffold/GTPase activity. These novel aspects of peripheral LRRK2 biology critically impact ongoing attempts to develop LRRK2 selective kinase inhibitors as therapeutics for PD

Mottness at finite doping and charge instabilities in cuprates

The intrinsic instability of underdoped copper oxides towards inhomogeneous states is one of the central puzzles of the physics of correlated materials. The influence of the Mott physics on the doping-temperature phase diagram of copper oxides represents a major issue that is subject of intense theoretical and experimental effort. Here, we investigate the ultrafast electron dynamics in prototypical single-layer Bi-based cuprates at the energy scale of the O-2p\u2192Cu-3d charge-transfer (CT) process. We demonstrate a clear evolution of the CT excitations from incoherent and localized, as in a Mott insulator, to coherent and delocalized, as in a conventional metal. This reorganization of the high-energy degrees of freedom occurs at the critical doping pcr 430.16 irrespective of the temperature, and it can be well described by dynamical mean field theory calculations. We argue that the onset of the low-temperature charge instabilities is the low-energy manifestation of the underlying Mottness that characterizes the p<pcr region of the phase diagram. This discovery sets a new framework for theories of charge order and low-temperature phases in underdoped copper oxides. ArXI