Model of Competencies for Decomposition of Human Behavior: Application to Control System of Robots

Humans and machines have shared the same physical space for many years. To share the same space, we want the robots to behave like human beings. This will facilitate their social integration, their interaction with humans and create an intelligent behavior. To achieve this goal, we need to understand how human behavior is generated, analyze tasks running our nerves and how they relate to them. Then and only then can we implement these mechanisms in robotic beings. In this study, we propose a model of competencies based on human neuroregulator system for analysis and decomposition of behavior into functional modules. Using this model allow separate and locate the tasks to be implemented in a robot that displays human-like behavior. As an example, we show the application of model to the autonomous movement behavior on unfamiliar environments and its implementation in various simulated and real robots with different physical configurations and physical devices of different nature. The main result of this study has been to build a model of competencies that is being used to build robotic systems capable of displaying behaviors similar to humans and consider the specific characteristics of robots.

The developmental control of size in insects

The mechanisms that control the sizes of a body and its many parts remain among the great puzzles in developmental biology. Why do animals grow to a species-specific body size, and how is the relative growth of their body parts controlled to so they grow to the right size, and in the correct proportion with body size, giving an animal its species-characteristic shape? Control of size must involve mechanisms that somehow assess some aspect of size and are upstream of mechanisms that regulate growth. These mechanisms are now beginning to be understood in the insects, in particular in Manduca sexta and Drosophila melanogaster. The control of size requires control of the rate of growth and control of the cessation of growth. Growth is controlled by genetic and environmental factors. Insulin and ecdysone, their receptors, and intracellular signaling pathways are the principal genetic regulators of growth. The secretion of these growth hormones, in turn, is controlled by complex interactions of other endocrine and molecular mechanisms, by environmental factors such as nutrition, and by the physiological mechanisms that sense body size. Although the general mechanisms of growth regulation appear to be widely shared, the mechanisms that regulate final size can be quite diverse.

Mollusca Non-Grata: The influence of top-down control and residence time on the abundance, distribution, and behavior of non-native marine snails in Washington State

Thesis (Ph.D.)--University of Washington, 2016-06

Mitochondrial control region diversity of the houbara bustard Chlamydotis undulata complex and genetic structure along the Atlantic seaboard of North Africa

The houbara bustard, Chlamydotis undulata, is a declining cryptic desert bird whose range extends from North Africa to Central Asia. Three subspecies are currently recognized by geographical distribution and morphology: C.u.fuertaventurae, C.u.undulata and C.u.macqueenii. We have sequenced 854 bp of mitochondrial control region from 73 birds to describe their population genetic structure with a particular sampling focus on the connectivity between C.u.fuertaventurae and C.u.undulata along the Atlantic seaboard of North Africa. Nucleotide and haplotypic diversity varied among the subspecies being highest in C.u.undulata, lowest in C.u.fuertaventurae and intermediate in C.u.macqueenii. C.u.fuertaventurae and C.u.undulata are paraphyletic and an average nucleotide divergence of 2.08% splits the later from C.u.macqueenii. We estimate that C.u.fuertaventurae and C.u.undulata split from C.u.macqueenii approximately 430 000 years ago. C.u.fuertaventurae and C.u.undulata are weakly differentiated (F-ST = 0.27, N-m = 1.3), indicative of a recent shared history. Archaeological evidence indicates that houbara bustards have been present on the Canary Islands for 130-170 000 years. However, our genetic data point to a more recent separation of C.u.fuertaventurae and C.u.undulata at around 20-25 000 years. Concordant archaeological, climatic opportunities for colonization and genetic data point to a scenario of: (i) initial colonization of the Canary Islands about 130 000 years ago; (ii) a period of secondary contact 19-30 000 years ago homogenizing any pre-existing genetic structure followed by; (iii) a period of relative isolation that persists today.

Hypothalamic control of bone formation: Distinct actions of leptin and Y2 receptor pathways

Leptin and Y2 receptors on hypothalamic NPY neurons mediate leptin effects on energy homeostasis; however, their interaction in modulating osteoblast activity is not established. Here, direct testing of this possibility indicates distinct mechanisms of action for leptin anti-osteogenic and Y2(-/-) anabolic pathways in modulating bone formation. Introduction: Central enhancement of bone formation by hypothalamic neurons is observed in leptin-deficient oblob and Y2 receptor null mice. Similar elevation in central neuropeptide Y (NPY) expression and effects on osteoblast activity in these two models suggest a shared pathway between leptin and Y2 receptors in the central control of bone physiology. The aim of this study was to test whether the leptin and Y2 receptor pathways regulate bone by the same or distinct mechanisms. Materials and Methods: The interaction of concomitant leptin and Y2 receptor deficiency in controlling bone was examined in Y2(-/-) oblob double mutant mice, to determine whether leptin and Y2 receptor deficiency have additive effects. Interaction between leptin excess and Y2 receptor deletion was examined using recombinant adeno-associated viral vector overproduction of NPY (AAV-NPY) to produce weight gain and thus leptin excess in adult Y2(-/-) mice. Cancellous bone volume and bone cell function were assessed. Results: Osteoblast activity was comparably elevated in oblob, Y2(-/-), and Y2(-/-) oblob mice. However, greater bone resorption in oblob and Y2(-/-) oblob mice reduced cancellous bone volume compared with Y2(-/-). Both wildtype and Y2(-/-) AAV-NPY mice exhibited marked elevation of white adipose tissue accumulation and hence leptin expression, thereby reducing osteoblast activity. Despite this anti-osteogenic leptin effect in the obese AAV-NPY model, osteoblast activity in Y2(-/-) AAV-NPY mice remained significantly greater than in wildtype AAV-NPY mice. Conclusions: This study suggests that NPY is not a key regulator of the leptin-dependent osteoblast activity, because both the leptin-deficient stimulation of bone formation and the excess leptin inhibition of bone formation can occur in the presence of high hypothalamic NPY. The Y2(-/-) pathway acts consistently to stimulate bone formation; in contrast, leptin continues to suppress bone formation as circulating levels increase. As a result, they act increasingly in opposition as obesity becomes more marked. Thus, in the absence of leptin, the cancellous bone response to loss of Y2 receptor and leptin activity can not be distinguished. However, as leptin levels increase to physiological levels, distinct signaling pathways are revealed.

Targeting the glycoprotein 130 receptor subunit to control pain and inflammation

The glycoprotein 130 (gp130) is a shared signal-transducing-membrane-associated receptor for several hematopoietic cytokines. Its activation is implicated in pain and in a variety of diseases via signaling of proinflammatory cytokines. These include interleukin-6 (IL-6) subfamily cytokines, many of which play important roles in the pathogenesis of diseases such as rheumatoid arthritis, Castleman's disease, and Kaposi's sarcoma. Several strategies have been developed to block gp130-receptor-mediated signaling. These include the application of monoclonal antibodies, the creation of mutant form(s) of the gp130 with increased binding affinity for such ligands as IL-6/sIL-6R complex, and the generation of antagonists by selective mutagenesis of the specific cytokine/gp130 receptor binding site(s). Other strategies include targeting gp130-mediated signaling pathways such as that involving signal transducer and activator of transcription-3. This review provides a summary of the latest research pertaining to the role of gp130 in the pathogenesis of inflammatory and other diseases in which the gp130 receptor is implicated. An overview of antagonists targeting the gp130 receptor is included with particular emphasis on their mechanism of action and their limitations and potential for therapeutic application.

Shared action spaces:a basis function framework for social re-calibration of sensorimotor representations supporting joint action

The article explores the possibilities of formalizing and explaining the mechanisms that support spatial and social perspective alignment sustained over the duration of a social interaction. The basic proposed principle is that in social contexts the mechanisms for sensorimotor transformations and multisensory integration (learn to) incorporate information relative to the other actor(s), similar to the "re-calibration" of visual receptive fields in response to repeated tool use. This process aligns or merges the co-actors' spatial representations and creates a "Shared Action Space" (SAS) supporting key computations of social interactions and joint actions; for example, the remapping between the coordinate systems and frames of reference of the co-actors, including perspective taking, the sensorimotor transformations required for lifting jointly an object, and the predictions of the sensory effects of such joint action. The social re-calibration is proposed to be based on common basis function maps (BFMs) and could constitute an optimal solution to sensorimotor transformation and multisensory integration in joint action or more in general social interaction contexts. However, certain situations such as discrepant postural and viewpoint alignment and associated differences in perspectives between the co-actors could constrain the process quite differently. We discuss how alignment is achieved in the first place, and how it is maintained over time, providing a taxonomy of various forms and mechanisms of space alignment and overlap based, for instance, on automaticity vs. control of the transformations between the two agents. Finally, we discuss the link between low-level mechanisms for the sharing of space and high-level mechanisms for the sharing of cognitive representations. © 2013 Pezzulo, Iodice, Ferraina and Kessler.

Adaptive control of hybrid battery energy storage systems under capacity fade

There is an increasing call for applications which use a mixture of batteries. These hybrid battery solutions may contain different battery types for example; using second life ex-transportation batteries in grid support applications or a combination of high power, low energy and low power, high energy batteries to meet multiple energy requirements or even the same battery types but under different states of health for example, being able to hot swap out a battery when it has failed in an application without changing all the batteries and ending up with batteries with different performances, capacities and impedances. These types of applications typically use multi-modular converters to allow hot swapping to take place without affecting the overall performance of the system. A key element of the control is how the different battery performance characteristics may be taken into account and the how the power is then shared among the different batteries in line with their performance. This paper proposes a control strategy which allows the power in the batteries to be effectively distributed even under capacity fade conditions using adaptive power sharing strategy. This strategy is then validated against a system of three different battery types connected to a multi-modular converter both with and without capacity fade mechanisms in place.

Multiple roles for executive control in belief-desire reasoning:distinct neural networks are recruited for self perspective inhibition and complexity of reasoning

Belief-desire reasoning is a core component of 'Theory of Mind' (ToM), which can be used to explain and predict the behaviour of agents. Neuroimaging studies reliably identify a network of brain regions comprising a 'standard' network for ToM, including temporoparietal junction and medial prefrontal cortex. Whilst considerable experimental evidence suggests that executive control (EC) may support a functioning ToM, co-ordination of neural systems for ToM and EC is poorly understood. We report here use of a novel task in which psychologically relevant ToM parameters (true versus false belief; approach versus avoidance desire) were manipulated orthogonally. The valence of these parameters not only modulated brain activity in the 'standard' ToM network but also in EC regions. Varying the valence of both beliefs and desires recruits anterior cingulate cortex, suggesting a shared inhibitory component associated with negatively valenced mental state concepts. Varying the valence of beliefs additionally draws on ventrolateral prefrontal cortex, reflecting the need to inhibit self perspective. These data provide the first evidence that separate functional and neural systems for EC may be recruited in the service of different aspects of ToM.

Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome.

The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.

STATE OF CHARGE BALANCING DROOP CONTROL

This thesis presents a load sharing method applied in a distributed micro grid system. The goal of this method is to balance the state-of-charge (SoC) of each parallel connected battery and make it possible to detect the average SoC of the system by measuring bus voltage for all connected modules. In this method the reference voltage for each battery converter is adjusted by adding a proportional SoC factor. Under such setting the battery with a higher SoC will output more power, whereas the one with lower SoC gives out less. Therefore the higher SoC battery will use its energy faster than the lower ones, and eventually the SoC and output power of each battery will converge. And because the reference voltage is related to SoC status, the information of the average SoC in this system could be shared for all modules by measuring bus voltage. The SoC balancing speed is related to the SoC droop factors. This SoC-based load sharing control system is analyzed in feasibility and stability. Simulations in MATLAB/Simulink are presented, which indicate that this control scheme could balance the battery SoCs as predicted. The observation of SoC sharing through bus voltage was validated in both software simulation and hardware experiments. It could be of use to non-communicated distributed power system in load shedding and power planning.

Hypothalamic Inflammation And The Central Nervous System Control Of Energy Homeostasis.

The control of energy homeostasis relies on robust neuronal circuits that regulate food intake and energy expenditure. Although the physiology of these circuits is well understood, the molecular and cellular response of this program to chronic diseases is still largely unclear. Hypothalamic inflammation has emerged as a major driver of energy homeostasis dysfunction in both obesity and anorexia. Importantly, this inflammation disrupts the action of metabolic signals promoting anabolism or supporting catabolism. In this review, we address the evidence that favors hypothalamic inflammation as a factor that resets energy homeostasis in pathological states.

Chitosan/tripolyphosphate Nanoparticles Loaded With Paraquat Herbicide: An Environmentally Safer Alternative For Weed Control.

Paraquat is a fast acting nonselective contact herbicide that is extensively used worldwide. However, the aqueous solubility and soil sorption of this compound can cause problems of toxicity in nontarget organisms. This work investigates the preparation and characterization of nanoparticles composed of chitosan and sodium tripolyphosphate (TPP) to produce an efficient herbicidal formulation that was less toxic and could be used for safer control of weeds in agriculture. The toxicities of the formulations were evaluated using cell culture viability assays and the Allium cepa chromosome aberration test. The herbicidal activity was investigated in cultivations of maize (Zea mays) and mustard (Brassica sp.), and soil sorption of the nanoencapsulated herbicide was measured. The efficiency association of paraquat with the nanoparticles was 62.6 ± 0.7%. Encapsulation of the herbicide resulted in changes in its diffusion and release as well as its sorption by soil. Cytotoxicity and genotoxicity assays showed that the nanoencapsulated herbicide was less toxic than the pure compound, indicating its potential to control weeds while at the same time reducing environmental impacts. Measurements of herbicidal activity showed that the effectiveness of paraquat was preserved after encapsulation. It was concluded that the encapsulation of paraquat in nanoparticles can provide a useful means of reducing adverse impacts on human health and the environment, and that the formulation therefore has potential for use in agriculture.

Influence Of Gastric Emptying On The Control Of Postprandial Glycemia: Physiology And Therapeutic Implications.

The maintenance of glucose homeostasis is complex and involves, besides the secretion and action of insulin and glucagon, a hormonal and neural mechanism, regulating the rate of gastric emptying. This mechanism depends on extrinsic and intrinsic factors. Glucagon-like peptide-1 secretion regulates the speed of gastric emptying, contributing to the control of postprandial glycemia. The pharmacodynamic characteristics of various agents of this class can explain the effects more relevant in fasting or postprandial glucose, and can thus guide the individualized treatment, according to the clinical and pathophysiological features of each patient.

Ki-1/57 And Cgi-55 Ectopic Expression Impact Cellular Pathways Involved In Proliferation And Stress Response Regulation.

Ki-1/57 (HABP4) and CGI-55 (SERBP1) are regulatory proteins and paralogs with 40.7% amino acid sequence identity and 67.4% similarity. Functionally, they have been implicated in the regulation of gene expression on both the transcriptional and mRNA metabolism levels. A link with tumorigenesis is suggested, since both paralogs show altered expression levels in tumor cells and the Ki-1/57 gene is found in a region of chromosome 9q that represents a haplotype for familiar colon cancer. However, the target genes regulated by Ki-1/57 and CGI-55 are unknown. Here, we analyzed the alterations of the global transcriptome profile after Ki-1/57 or CGI-55 overexpression in HEK293T cells by DNA microchip technology. We were able to identify 363 or 190 down-regulated and 50 or 27 up-regulated genes for Ki-1/57 and CGI-55, respectively, of which 20 were shared between both proteins. Expression levels of selected genes were confirmed by qRT-PCR both after protein overexpression and siRNA knockdown. The majority of the genes with altered expression were associated to proliferation, apoptosis and cell cycle control processes, prompting us to further explore these contexts experimentally. We observed that overexpression of Ki-1/57 or CGI-55 results in reduced cell proliferation, mainly due to a G1 phase arrest, whereas siRNA knockdown of CGI-55 caused an increase in proliferation. In the case of Ki-1/57 overexpression, we found protection from apoptosis after treatment with the ER-stress inducer thapsigargin. Together, our data give important new insights that may help to explain these proteins putative involvement in tumorigenic events.