A neural integrator model for planning and value-based decision making of a robotics assistant

Modern manufacturing and assembly environments are characterized by a high variability in the built process which challenges human–robot cooperation. To reduce the cognitive workload of the operator, the robot should not only be able to learn from experience but also to plan and decide autonomously. Here, we present an approach based on Dynamic Neural Fields that apply brain-like computations to endow a robot with these cognitive functions. A neural integrator is used to model the gradual accumulation of sensory and other evidence as time-varying persistent activity of neural populations. The decision to act is modeled by a competitive dynamics between neural populations linked to different motor behaviors. They receive the persistent activation pattern of the integrators as input. In the first experiment, a robot learns rapidly by observation the sequential order of object transfers between an assistant and an operator to subsequently substitute the assistant in the joint task. The results show that the robot is able to proactively plan the series of handovers in the correct order. In the second experiment, a mobile robot searches at two different workbenches for a specific object to deliver it to an operator. The object may appear at the two locations in a certain time period with independent probabilities unknown to the robot. The trial-by-trial decision under uncertainty is biased by the accumulated evidence of past successes and choices. The choice behavior over a longer period reveals that the robot achieves a high search efficiency in stationary as well as dynamic environments.The work received financial support from FCT through the PhD fellowships PD/BD/128183/2016 and SFRH/BD/124912/2016, the project “Neurofield” (PTDC/MAT-APL/31393/2017) and the research centre CMAT within the project UID/MAT/00013/2013

Emotional design and human-robot interaction

Recent years have shown an increase in the importance of emotions applied to the Design field - Emotional Design. In this sense, the emotional design aims to elicit (e.g., pleasure) or prevent (e.g., displeasure) determined emotions, during human product interaction. That is, the emotional design regulates the emotional interaction between the individual and the product (e.g., robot). Robot design has been a growing area whereby robots are interacting directly with humans in which emotions are essential in the interaction. Therefore, this paper aims, through a non-systematic literature review, to explore the application of emotional design, particularly on Human-Robot Interaction. Robot design features (e.g., appearance, expressing emotions and spatial distance) that affect emotional design are introduced. The chapter ends with a discussion and a conclusion.info:eu-repo/semantics/acceptedVersio

LunaRoo: A proposal for the Google Lunar XPrize payload opportunity with the part time scientists team

This proposal describes the innovative and competitive lunar payload solution developed at the Queensland University of Technology (QUT)–the LunaRoo: a hopping robot designed to exploit the Moon's lower gravity to leap up to 20m above the surface. It is compact enough to fit within a 10cm cube, whilst providing unique observation and mission capabilities by creating imagery during the hop. This first section is deliberately kept short and concise for web submission; additional information can be found in the second chapter

Challenges associated with CRISPR-Cas antimicrobials and potential routes to overcome them.

<p>A summary of the obstacles associated with using CRISPR-Cas–based antimicrobials in complex environmental populations of bacteria is shown. These include ensuring effective delivery of constructs (top left), routes of resistance evolution to these novel antimicrobials (top right), the species diversity and spatial complexity of bacterial communities (bottom left), and uncertainty in usage guidelines and stakeholder support (bottom right). AMR, antimicrobial resistance; CRISPR-Cas, clustered regularly interspaced short palindromic repeats-CRISPR–associated.</p

Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine

Endogenous circadian clocks regulate 24-h rhythms of physiology and behavior. Circadian rhythm disruption (CRD) is suggested as a risk factor for inflammatory bowel disease. However, the underlying molecular mechanisms remain unknown. Intestinal biopsies from Per1/2 mutant and wild-type (WT) mice were investigated by electron microscopy, immunohistochemistry, and bromodeoxyuridine pulse-chase experiments. TNF-alpha was injected intraperitoneally, with or without necrostatin-1, into Per1/2 mice or rhythmic and externally desynchronized WT mice to study intestinal epithelial cell death. Experimental chronic colitis was induced by oral administration of dextran sodium sulfate. In vitro, caspase activity was assayed in Per1/2-specific small interfering RNA-transfected cells. Wee1 was overexpressed to study antiapoptosis and the cell cycle. Genetic ablation of circadian clock function or environmental CRD in mice increased susceptibility to severe intestinal inflammation and epithelial dysregulation, accompanied by excessive necroptotic cell death and a reduced number of secretory epithelial cells. Receptor-interacting serine/threonine-protein kinase (RIP)-3-mediated intestinal necroptosis was linked to increased mitotic cell cycle arrest via Per1/2-controlled Wee1, resulting in increased antiapoptosis via cellular inhibitor of apoptosis-2. Together, our data suggest that circadian rhythm stability is pivotal for the maintenance of mucosal barrier function. CRD increases intestinal necroptosis, thus rendering the gut epithelium more susceptible to inflammatory processes

Thermoneutral housing exacerbates nonalcoholic fatty liver disease in mice and allows for sex-independent disease modeling.

Nonalcoholic fatty liver disease (NAFLD), a common prelude to cirrhosis and hepatocellular carcinoma, is the most common chronic liver disease worldwide. Defining the molecular mechanisms underlying the pathogenesis of NAFLD has been hampered by a lack of animal models that closely recapitulate the severe end of the disease spectrum in humans, including bridging hepatic fibrosis. Here we demonstrate that a novel experimental model employing thermoneutral housing, as opposed to standard housing, resulted in lower stress-driven production of corticosterone, augmented mouse proinflammatory immune responses and markedly exacerbated high-fat diet (HFD)-induced NAFLD pathogenesis. Disease exacerbation at thermoneutrality was conserved across multiple mouse strains and was associated with augmented intestinal permeability, an altered microbiome and activation of inflammatory pathways that are associated with the disease in humans. Depletion of Gram-negative microbiota, hematopoietic cell deletion of Toll-like receptor 4 (TLR4) and inactivation of the IL-17 axis resulted in altered immune responsiveness and protection from thermoneutral-housing-driven NAFLD amplification. Finally, female mice, typically resistant to HFD-induced obesity and NAFLD, develop full disease characteristics at thermoneutrality. Thus, thermoneutral housing provides a sex-independent model of exacerbated NAFLD in mice and represents a novel approach for interrogation of the cellular and molecular mechanisms underlying disease pathogenesis