A model of symbiomemesis: machine education and communication as pillars for human-autonomy symbiosis.

Symbiosis is a physiological phenomenon where organisms of different species develop social interdependencies through partnerships. Artificial agents need mechanisms to build their capacity to develop symbiotic relationships. In this paper, we discuss two pillars for these mechanisms: machine education (ME) and bi-directional communication. ME is a new revolution in artificial intelligence (AI) which aims at structuring the learning journey of AI-enabled autonomous systems. In addition to the design of a systematic curriculum, ME embeds the body of knowledge necessary for the social integration of AI, such as ethics, moral values and trust, into the evolutionary design and learning of the AI. ME promises to equip AI with skills to be ready to develop logic-based symbiosis with humans and in a manner that leads to a trustworthy and effective steady-state through the mental interaction between humans and autonomy; a state we name symbiomemesis to differentiate it from ecological symbiosis. The second pillar, bi-directional communication as a discourse enables information to flow between the AI systems and humans. We combine machine education and communication theory as the two prerequisites for symbiosis of AI agents and present a formal computational model of symbiomemesis to enable symbiotic human-autonomy teaming. This article is part of the theme issue 'Towards symbiotic autonomous systems'.

Network motifs for translator stylometry identification.

Despite the extensive literature investigating stylometry analysis in authorship attribution research, translator stylometry is an understudied research area. The identification of translator stylometry contributes to many fields including education, intellectual property rights and forensic linguistics. In a two stage process, this paper first evaluates the use of existing lexical measures for the translator stylometry problem. Similar to previous research we found that using vocabulary richness in its traditional form as it has been used in the literature could not identify translator stylometry. This encouraged us to design an approach with the aim of identifying the distinctive patterns of a translator by employing network-motifs. Networks motifs are small sub-graphs which aim at capturing the local structure of a complex network. The proposed approach achieved an average accuracy of 83% in three-way classification. These results demonstrate that classic tools based on lexical features can be used for identifying translator stylometry if they get augmented with appropriate non-parametric scaling. Moreover, the use of complex network analysis and network motifs mining provided made it possible to design features that can solve translator stylometry analysis problems.

When is altruistic punishment useful in social dilemmas?

It is not fully understood how cooperation emerges in a population of individuals with no connections or prior experience with each other. Strategy selection that is purely based on accumulated payoffs promotes free riders who put their self interests above that of any group. How could cooperation persist in these settings? Researchers have posited direct or indirect reciprocity as possible explanations but these theories fail if interactions are not repeated or reputations are ignored. Altruistic punishment may provide an answer. Punishers impose a penalty, such as a fine, on defectors. The idea is a sufficiently high enough penalty-or even the threat of a high penalty-will convince defectors that cooperation is more beneficial. The punishment is altruistic because punishers pay a cost to impose a penalty and expect nothing in return (including no future reciprocity). Empirical and human studies have shown when some individuals are punishers, and they are common, cooperation levels tend to increase. But it has never been specified exactly how large this majority of punishers must be to promote cooperation. Here we analyze cooperation, defection and punishment in a social dilemma, public goods game, and precisely identify the necessary conditions to make altruistic punishment an effective strategy for improving group cooperation levels.

Trusted Autonomy and Cognitive Cyber Symbiosis: Open Challenges.

This paper considers two emerging interdisciplinary, but related topics that are likely to create tipping points in advancing the engineering and science areas. Trusted Autonomy (TA) is a field of research that focuses on understanding and designing the interaction space between two entities each of which exhibits a level of autonomy. These entities can be humans, machines, or a mix of the two. Cognitive Cyber Symbiosis (CoCyS) is a cloud that uses humans and machines for decision-making. In CoCyS, human-machine teams are viewed as a network with each node comprising humans (as computational machines) or computers. CoCyS focuses on the architecture and interface of a Trusted Autonomous System. This paper examines these two concepts and seeks to remove ambiguity by introducing formal definitions for these concepts. It then discusses open challenges for TA and CoCyS, that is, whether a team made of humans and machines can work in fluid, seamless harmony.

Dysregulated production of interleukin-1ß upon activation of the NLRP3 inflammasome in patients with familial Mediterranean fever.

Familial Mediterranean fever (FMF) is caused by mutations in pyrin, a protein expressed in innate immune cells that interacts with caspase-1 and other inflammasome components to regulate interleukin (IL)-1ß maturation. Since NLRP3 inflammasome represents major source of IL-1ß, we studied its protein expression and function in FMF. We isolated peripheral white blood cells (WBCs) from 20 symptoms-free FMF patients and 21 healthy individuals. Intracellular protein expression of NLRP3, caspase-1, IL-1ß at baseline and after LPS/ATP sequential treatment for NLRP3 activation was assessed by immunoblotting. Secreted IL-1ß was quantified by ELISA. THP-1 cells were transfected with wild-type or mutant pyrin and IL-1ß secretion was measured. FMF WBCs exhibited lower NLRP3 and active caspase-1 protein expression compared to healthy individuals, and LPS/ATP treatment resulted in significantly lower intracellular IL-1ß levels in FMF patients. Likewise, LPS/ATP induced caspase-1-dependent IL-1ß release at significantly lower amounts in the FMF group (1182±192 versus 2134±245pg/mL in controls, p=0.004). Consistently, THP-1 cells transfected with FMF-associated M694V mutant pyrin displayed lower LPS/ATP-induced IL-1ß compared with wild-type pyrin-transfected cells. FMF WBCs demonstrate reduced NLRP3-mediated IL-1ß production. Additional studies are needed to define whether this finding represents a compensatory mechanism to control inflammation or is directly linked to disease pathogenesis.

The role of the pro-apoptotic protein Siva in the pathogenesis of Familial Mediterranean fever: A structural and functional analysis.

Familial Mediterranean fever (FMF) is an autosomal, recessive disease, attributed to mutations in MEFV gene encoding pyrin, which is characterized by recurrent, acute and self-limiting attacks of fever as well as an increased neutrophil and monocyte apoptosis. Most disease-associated mutations in MEFV gene reside on the C-terminal PRYSPRY (B30.2) domain of pyrin, an area found to interact with the pro-apoptotic protein Siva. Because apoptotic events may be contributing to endogenous inflammation we hypothesized that mutations in pyrin may affect Siva-mediated apoptosis. The confirmation of this hypothesis would be of a great biological significance since it would be demonstrated a connection between apoptosis and inflammation. We used homology modeling to construct a 3-D model of Siva protein and the constructed model of Siva defined structural elements with potential of binding other proteins to induce apoptosis. Given that Siva protein binds pyrin as shown by transfection and immunoprecipitation experiments, apoptosis was assessed by FACS and Western blotting. No differences in rates of apoptosis in myeloid cells (THP-1) upon transfection with either wt pyrin or mutant forms of pyrin were found. Patients with FMF did not display any mutations in the Siva-1 (full length) gene. Siva-1 was not linked to pyrin in the major predicted FMF gene network constructed using a literature-curated gene signature for FMF. These results suggest that Siva-mediated unprovoked apoptosis is not likely to be involved in the pathogenesis of FMF.

Vitamin D receptor gene polymorphisms and susceptibility to type 1 diabetes in Crete, Greece.

INTRODUCTION: Association studies of vitamin D receptor (VDR) polymorphisms and risk of type 1 diabetes (T1D) have produced inconsistent results in different populations, pointing to contribution of additional genetic variants and environmental factors. In this study we investigated the association between four VDR polymorphisms and susceptibility to T1D in Crete, an island with homogenous population and considerably low incidence of T1D. RESULTS AND DISCUSSION: We genotyped 100 patients with T1D and 96 controls for the FokI (rs10735810), BsmI (rs1544410), ApaI (rs7975232), and TaqI (rs731236) single nucleotide polymorphisms by polymerase chain reaction and restriction fragment length polymorphism analysis. In all 4 polymorphisms tested, distribution of VDR genotype frequencies differed significantly between patients and controls. Individuals with T1D presented less commonly with FokI F allele (p=0.008; OR 0.52, 95% CI 0.32 to 0.85) and BsmI B allele (p=0.042; OR 0.65, 95% CI 0.44 to 0.97) and more commonly with ApaI A allele (p=0.024; OR 1.61, 95% CI 1.07 to 2.41) and TaqI T allele (p=0.0001; OR 2.24, 95% CI 1.49 to 3.36). CONCLUSION: Our findings derived from a homogenous southern European population with low incidence of T1D suggest that FokI, BsmI, ApaI, and TaqI polymorphisms of the VDR gene are associated with T1D prevalence.

Association of a TRAF1 and a STAT4 gene polymorphism with increased risk for rheumatoid arthritis in a genetically homogeneous population.

Rheumatoid arthritis (RA) is a multifactorial disease that is increasing in incidence worldwide. It is associated with a complex mode of inheritance, with many genes being involved in the development and progression of the disease. Genome-wide association studies in different populations have recently revealed a significant association between a TRAF1/C5 and a STAT4 polymorphism and the development of RA. In the present study we performed a case-control study in the population of the island of Crete, Greece, aiming to replicate the former findings in a genetically homogeneous cohort of patients. We found that mutated allele A or genotypes A/A and G/A of the TRAF1/C5 rs10818488 SNP were more common in individuals with RA than in control individuals (odds ratio [OR]=1.7, 95% confidence interval [CI]=1.35-2.15, and OR=2.22, 95% CI=1.61-3.05, respectively). Similarly, mutated allele T or genotypes T/T and G/T of the STAT4 rs7574865 SNP were also associated with susceptibility to RA (OR=1.9, 95% CI=1.46-2.50, and OR=2.37, 95% CI 1.73-2.25, respectively). Thus, we conclude that mutant alleles or genotypes of both polymorphisms examined are associated with the development of RA in our population.

Intron 4 a/b polymorphism of the endothelial nitric oxide synthase gene is associated with both type 1 and type 2 diabetes in a genetically homogeneous population.

Current classifications of diabetes distinguish between type 1 diabetes (T1D) and type 2 diabetes (T2D), however recent evidence highlights overlap between T1D and T2D. Earlier studies have suggested altered nitric oxide (NO) metabolism in both T1D and T2D. In the present case-control study, we investigated whether the endothelial NO synthase gene intron 4 a/b polymorphism is associated with T1D and T2D in the island of Crete, a well-defined area with genetically homogeneous population. Mutated allele "a" was more common in individuals with both T1D and T2D than in controls (odds ratio [OR] = 1.71, 95% confidence interval [CI] = 1.06-2.77, p = 0.013; and OR = 1.50, 95% CI = 0.930-2.42, p = 0.047, respectively). Mutated genotype (a/a or a/b) was more common in individuals with T1D than in nondiabetic individuals (OR = 1.93, 95% CI = 1.12-3.32, p = 0.008); this increased frequency was also observed for T2D, although not at a significant level (OR = 1.38, 95% CI = 0.802-2.37). No difference was found in the frequency of mutated allele a or mutated genotype (a/a or a/b) between T1D and T2D populations. In conclusion, our results indicate that allele a of the intron 4 endothelial NO synthase gene is associated with susceptibility to both T1D and T2D and may represent a common genetic factor for diabetes.