A flexible component-based robot control architecture for hormonal modulation of behaviour and affect

This document is the Accepted Manuscritpt of a paper published in Proceedings of 18th Annual Conference, TAROS 2017, Guildford, UK, July 19–21, 2017. Under embargo. Embargo end date: 20 July 2018. The final publication is available at Springer via https://link.springer.com/chapter/10.1007%2F978-3-319-64107-2_36. © 2017 Springer, Cham.In this paper we present the foundations of an architecture that will support the wider context of our work, which is to explore the link between affect, perception and behaviour from an embodied perspective and assess their relevance to Human Robot Interaction (HRI). Our approach builds upon existing affect-based architectures by combining artificial hormones with discrete abstract components that are designed with the explicit consideration of influencing, and being receptive to, the wider affective state of the robot

Discursos técnico-científicos en la construcción social y política de la Reserva de la Biósfera de la Sierra Gorda en Querétaro

Los estados-nación modernos han adoptado el modelo de Reservas de la Biósfera como la herramienta política por excelencia para la conservación de la biodiversidad. Estos espacios naturales son concebidos desde una lógica de racionalidad moderna donde el conocimiento técnico-científico ocupa un papel central en la gestión. Aunque los gestores requieren del conocimiento que producen los académicos para llevar a cabo su labor y viceversa, en la Reserva de la Biósfera de la Sierra Gorda queretana, el conocimiento técnico-científico producido por la academia es percibido como algo ajeno y fuera de la realidad, mientras que los académicos de la Universidad Autónoma de Querétaro consideran que no se está llevando a cabo una gestión adecuada de la Reserva. Es justamente en esta disputa entre saberes modernos donde se sitúan los aportes de esta tesis. Los resultados se obtuvieron a través del análisis del discurso y de la Schemata de Praxis y dan cuenta de las visiones confrontadas que estos grupos tienen en torno a la naturaleza, al conocimiento técnico-científico y al desarrollo. El reflexionar sobre esta confrontación discursiva brinda elementos para establecer modelos de gestión centrados en el lugar que contribuyan a la construcción social y política de un medio ambiente donde los saberes híbridos puedan ocupar una posición más equitativa

Programmed cell senescence during mammalian embryonic development

Cellular senescence disables proliferation in damaged cells, and it is relevant for cancer and aging. Here, we show that senescence occurs during mammalian embryonic development at multiple locations, including the mesonephros and the endolymphatic sac of the inner ear, which we have analyzed in detail. Mechanistically, senescence in both structures is strictly dependent on p21, but independent of DNA damage, p53, or other cell-cycle inhibitors, and it is regulated by the TGF-beta/SMAD and PI3K/FOXO pathways. Developmentally programmed senescence is followed by macrophage infiltration, clearance of senescent cells, and tissue remodeling. Loss of senescence due to the absence of p21 is partially compensated by apoptosis but still results in detectable developmental abnormalities. Importantly, the mesonephros and endolymphatic sac of human embryos also show evidence of senescence. We conclude that the role of developmentally programmed senescence is to promote tissue remodeling and propose that this is the evolutionary origin of damage-induced senescence

Outline of a sensory-motor perspective on intrinsically moral agents

This is the accepted version of the following article: Christian Balkenius, Lola Cañamero, Philip Pärnamets, Birger Johansson, Martin V Butz, and Andreas Olson, ‘Outline of a sensory-motor perspective on intrinsically moral agents’, Adaptive Behaviour, Vol 24(5): 306-319, October 2016, which has been published in final form at DOI: https://doi.org/10.1177/1059712316667203 Published by SAGE ©The Author(s) 2016We propose that moral behaviour of artificial agents could (and should) be intrinsically grounded in their own sensory-motor experiences. Such an ability depends critically on seven types of competencies. First, intrinsic morality should be grounded in the internal values of the robot arising from its physiology and embodiment. Second, the moral principles of robots should develop through their interactions with the environment and with other agents. Third, we claim that the dynamics of moral (or social) emotions closely follows that of other non-social emotions used in valuation and decision making. Fourth, we explain how moral emotions can be learned from the observation of others. Fifth, we argue that to assess social interaction, a robot should be able to learn about and understand responsibility and causation. Sixth, we explain how mechanisms that can learn the consequences of actions are necessary for a robot to make moral decisions. Seventh, we describe how the moral evaluation mechanisms outlined can be extended to situations where a robot should understand the goals of others. Finally, we argue that these competencies lay the foundation for robots that can feel guilt, shame and pride, that have compassion and that know how to assign responsibility and blame.Peer reviewedFinal Accepted Versio

Affective Guide with Attitude

The Affective Guide System is a mobile context-aware and spatial-aware system, offering the user with an affective multimodal interaction interface. The system takes advantage of the current mobile and wireless technologies. It includes an ‘affective guide with attitude’ that links its memories and visitor’s interest to the spatial location so that stories are relevant to what can be immediately seen. This paper presents a review of related work, the system in detail, challenges and the future work to be carried out

Hedonic Quality or Reward? A Study of Basic Pleasure in Homeostasis and Decision Making of a Motivated Autonomous Robot

© The Author (s) 2016. Published by SAGE. This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).We present a robot architecture and experiments to investigate some of the roles that pleasure plays in the decision making (action selection) process of an autonomous robot that must survive in its environment. We have conducted three sets of experiments to assess the effect of different types of pleasure---related versus unrelated to the satisfaction of physiological needs---under different environmental circumstances. Our results indicate that pleasure, including pleasure unrelated to need satisfaction, has value for homeostatic management in terms of improved viability and increased flexibility in adaptive behavior.Peer reviewedFinal Published versio

CorE from Myxococcus xanthus Is a Copper-Dependent RNA Polymerase Sigma Factor

The dual toxicity/essentiality of copper forces cells to maintain a tightly regulated homeostasis for this metal in all living organisms, from bacteria to humans. Consequently, many genes have previously been reported to participate in copper detoxification in bacteria. Myxococcus xanthus, a prokaryote, encodes many proteins involved in copper homeostasis that are differentially regulated by this metal. A σ factor of the ECF (extracytoplasmic function) family, CorE, has been found to regulate the expression of the multicopper oxidase cuoB, the P1B-type ATPases copA and copB, and a gene encoding a protein with a heavy-metal-associated domain. Characterization of CorE has revealed that it requires copper to bind DNA in vitro. Genes regulated by CorE exhibit a characteristic expression profile, with a peak at 2 h after copper addition. Expression rapidly decreases thereafter to basal levels, although the metal is still present in the medium, indicating that the activity of CorE is modulated by a process of activation and inactivation. The use of monovalent and divalent metals to mimic Cu(I) and Cu(II), respectively, and of additives that favor the formation of the two redox states of this metal, has revealed that CorE is activated by Cu(II) and inactivated by Cu(I). The activation/inactivation properties of CorE reside in a Cys-rich domain located at the C terminus of the protein. Point mutations at these residues have allowed the identification of several Cys involved in the activation and inactivation of CorE. Based on these data, along with comparative genomic studies, a new group of ECF σ factors is proposed, which not only clearly differs mechanistically from the other σ factors so far characterized, but also from other metal regulators

Exploring the Gain of Function Contribution of AKT to Mammary Tumorigenesis in Mouse Models

Elevated expression of AKT has been noted in a significant percentage of primary human breast cancers, mainly as a consequence of the PTEN/PI3K pathway deregulation. To investigate the mechanistic basis of the AKT gain of function-dependent mechanisms of breast tumorigenesis, we explored the phenotype induced by activated AKT transgenes in a quantitative manner. We generated several transgenic mice lines expressing different levels of constitutively active AKT in the mammary gland. We thoroughly analyzed the preneoplastic and neoplastic mammary lesions of these mice and correlated the process of tumorigenesis to AKT levels. Finally, we analyzed the impact that a possible senescent checkpoint might have in the tumor promotion inhibition observed, crossing these lines to mammary specific p53(R172H) mutant expression, and to p27 knock-out mice. We analyzed the benign, premalignant and malignant lesions extensively by pathology and at molecular level analysing the expression of proteins involved in the PI3K/AKT pathway and in cellular senescence. Our findings revealed an increased preneoplastic phenotype depending upon AKT signaling which was not altered by p27 or p53 loss. However, p53 inactivation by R172H point mutation combined with myrAKT transgenic expression significantly increased the percentage and size of mammary carcinoma observed, but was not sufficient to promote full penetrance of the tumorigenic phenotype. Molecular analysis suggest that tumors from double myrAKT;p53(R172H) mice result from acceleration of initiated p53(R172H) tumors and not from bypass of AKT-induced oncogenic senescence. Our work suggests that tumors are not the consequence of the bypass of senescence in MIN. We also show that AKT-induced oncogenic senescence is dependent of pRb but not of p53. Finally, our work also suggests that the cooperation observed between mutant p53 and activated AKT is due to AKT-induced acceleration of mutant p53-induced tumors. Finally, our work shows that levels of activated AKT are not essential in the induction of benign or premalignant tumors, or in the cooperation of AKT with other tumorigenic signal such as mutant p53, once AKT pathway is activated, the relative level of activity seems not to determine the phenotype

Natural History of MYH7-Related Dilated Cardiomyopathy

BACKGROUND: Variants in myosin heavy chain 7 (MYH7) are responsible for disease in 1% to 5% of patients with dilated cardiomyopathy (DCM); however, the clinical characteristics and natural history of MYH7-related DCM are poorly described. OBJECTIVE: We sought to determine the phenotype and prognosis of MYH7-related DCM. We also evaluated the influence of variant location on phenotypic expression. METHODS: We studied clinical data from 147 individuals with DCM-causing MYH7 variants (47.6% female; 35.6 ± 19.2 years) recruited from 29 international centers. RESULTS: At initial evaluation, 106 (72.1%) patients had DCM (left ventricular ejection fraction: 34.5% ± 11.7%). Median follow-up was 4.5 years (IQR: 1.7-8.0 years), and 23.7% of carriers who were initially phenotype-negative developed DCM. Phenotypic expression by 40 and 60 years was 46% and 88%, respectively, with 18 patients (16%) first diagnosed at <18 years of age. Thirty-six percent of patients with DCM met imaging criteria for LV noncompaction. During follow-up, 28% showed left ventricular reverse remodeling. Incidence of adverse cardiac events among patients with DCM at 5 years was 11.6%, with 5 (4.6%) deaths caused by end-stage heart failure (ESHF) and 5 patients (4.6%) requiring heart transplantation. The major ventricular arrhythmia rate was low (1.0% and 2.1% at 5 years in patients with DCM and in those with LVEF of ≤35%, respectively). ESHF and major ventricular arrhythmia were significantly lower compared with LMNA-related DCM and similar to DCM caused by TTN truncating variants. CONCLUSIONS: MYH7-related DCM is characterized by early age of onset, high phenotypic expression, low left ventricular reverse remodeling, and frequent progression to ESHF. Heart failure complications predominate over ventricular arrhythmias, which are rare