Altruism in groups: an evolutionary games approach

We revisit in this paper the relation between evolution of species and the mathematical tool of evolutionary games, which has been used to model and predict it. We indicate known shortcoming of this model that restricts the capacity of evolutionary games to model groups of individuals that share a common gene or a common fitness function. In this paper we provide a new concept to remedy this shortcoming in the standard evolutionary games in order to cover this kind of behavior. Further, we explore the relationship between this new concept and Nash equilibrium or ESS. We indicate through the study of some example in the biology as Hawk and Dove game, Stag Hunt Game and Prisoner Dilemma, that when taking into account a utility that is common to a group of individuals, the equilibrium structure may change dramatically. We also study the multiple access control in slotted Aloha based wireless networks. We analyze the impact of the altruism behavior on the performance at the equilibrium

Relationship between biodiversity and agricultural production

International audienceThe intensification of agriculture is one of the main causes of biodiversity loss. We model the interdependent relationship between agriculture and wild biodiversity providing regulating services to agriculture on farmed land. We suppose that while agriculture has a negative impact on wild biodiversity, the latter can increase agricultural production. Farmers act as myopic agents, who maximize their instantaneous profit without considering the negative effects of their practice on the evolution of biodiversity. Two unexpected results arise (a) a tax on inputs can have a positive effect on yield since it can be considered as a social signal helping farmers to avoid myopic behavior concerning the positive effect of biodiversity on yield; (b) increasing biodiversity productivity, a proposal of ecological intensification, affects negatively the level of biodiversity, a counter‐intuitive result; due to the fact that when biodiversity is more productive, farmers can maintain lower biodiversity to get the same yield

Revisiting Evolutionary Game Theory

International audienceEvolutionary game theory is a relatively young mathematical theory that aims to formalize in mathematical terms evolution models in biology. In recent years this paradigm has penetrated more and more into other areas such as the linguistics, economics and engineering. The current theory of evolutionary game makes an implicit assumption that the evolution is driven by selfishness of individuals who interact with each others. In mathematical terms this can be stated as "an individual equals a player in a game model". This assumption turns out to be quite restrictive in modeling evolution in biology. It is now more and more accepted among biologist that the evolution is driven by the selfish interests of large groups of individuals; a group may correspond for example to a whole beehive or to an ants' nest. In this paper we propose an alternative paradigm for modeling evolution where a player does not necessarily represent an interacting individual but a whole class of such individuals

Pricing access to the Internet with partial information

International audienceWe shall consider two competition problems between service providers with asymmetric information. The utility of each one of them depends on the demand it gets and in its price. The demand itself is also a function of the prices of the providers. In both problems there is one provider (player 1) that has more information than the other (player 2) on the demand function. The more informed provider plays first, and then the second observes the move of the first provider and chooses accordingly its own action: it determines its price per unit demand. In the first problem that we consider, the first provider does not control its price (it has a fixed price known to the other provider which does not depend on the information that is unknown to provider 2). Before player 2 takes its action it receives a signal (or a recommendation) from the more informed player, i.e. from provider 1. The pure actions of provider 1 are thus the possible choices of what signal to send. The second problem that we consider is the same as the first one except that the actions of provider 1 is to choose its price. Since player 2 observes the choice of price of player 1 before it takes its own pricing decision, we can consider the choice of price by player 1 has also a role of signalling. We reduce each one of the problem to an equivalent four by four matrix game

State-Policy Dynamics in Evolutionary Games

International audienceStandard Evolutionary Game Theory framework is a useful tool to study large interacting systems and to understand the strategic behavior of individuals in such complex systems. Adding an individual state to model local feature of each player in this context, allows one to study a wider range of problems in various application areas as networking, biology, etc. In this paper, we introduce such an extension of evolutionary game framework and particularly, we focus on the dynamical aspects of this system. Precisely, we study the coupled dynamics of the policies and the individual states inside a population of interacting individuals. We first define a general model by coupling replicator dynamics and continuous-time Markov Decision Processes and we then consider a particular case of a two policies and two states evolutionary game. We first obtain a system of combined dynamics and we show that the rest-points of this system are equilibria profiles of our evolutionary game with individual state dynamics. Second, by assuming two different time scales between states and policies dynamics, we can compute explicitly the equilibria. Then, by transforming our evolutionary game with individual states into a standard evolutionary game, we obtain an equilibrium profile which is equivalent , in terms of occupation measures and expected fitness to the previous one. All our results are illustrated with numerical analysis

Altruism in groups

International audienceEvolutionary Game Theory has been originally developed and formalized by [247], in order to model the evolution of animal species and it has soon become an important mathematical tool to predict and even design evolution in many fields, others than biology. It mainly focuses on the dynamical evolution of the strategies adopted in a population of interacting individuals, where the notion of equilibrium adopted is that of Evolutionarily Stable Strategy (ESS, [247]), implying robustness against a mutation (i.e. a change in the strategy) of a small fraction of the population. This is a stronger condition than the standard Nash equilibrium concept, which requires robustness against deviation of a single user. On the importance of the ESS for understanding the evolution of species, Dawkins writes in his book "The Selfish Gene" [290]: "we may come to look back on the invention of the ESS concept as one of the most important advances in evolutionary theory since Darwin." He further specifies: "Maynard Smith's concept of the ESS will enable us, for the first time, to see clearly how a collection of independent selfish entities can come to resemble a single organized whole. Evolutionary game theory is nowadays considered as an important enrichment of game theory and it's applied in a wide variety of fields, spanning from social sciences [107] to computer science. Some examples of applications in computer science can be found in multiple access protocols [250], multihoming[240] and resources competition in the Internet [298]. This theory is usually adopted in situations where individuals belonging to a very large population are matched in random pairwise interactions. In classical evolutionary games (EG), each individual constitutes a selfish player involved in a non-cooperative game, maximizing its own utility, also said fitness, since in

The cAMP-HMGA1-RBP4 system: a novel biochemical pathway for modulating glucose homeostasis

<p>Abstract</p> <p>Background</p> <p>We previously showed that mice lacking the high mobility group A1 gene (<it>Hmga1</it>-knockout mice) developed a type 2-like diabetic phenotype, in which cell-surface insulin receptors were dramatically reduced (below 10% of those in the controls) in the major targets of insulin action, and glucose intolerance was associated with increased peripheral insulin sensitivity. This particular phenotype supports the existence of compensatory mechanisms of insulin resistance that promote glucose uptake and disposal in peripheral tissues by either insulin-dependent or insulin-independent mechanisms. We explored the role of these mechanisms in the regulation of glucose homeostasis by studying the <it>Hmga1</it>-knockout mouse model. Also, the hypothesis that increased insulin sensitivity in <it>Hmga1</it>-deficient mice could be related to the deficit of an insulin resistance factor is discussed.</p> <p>Results</p> <p>We first show that HMGA1 is needed for basal and cAMP-induced retinol-binding protein 4 (<it>RBP4</it>) gene and protein expression in living cells of both human and mouse origin. Then, by employing the <it>Hmga1</it>-knockout mouse model, we provide evidence for the identification of a novel biochemical pathway involving HMGA1 and the RBP4, whose activation by the cAMP-signaling pathway may play an essential role for maintaining glucose metabolism homeostasis <it>in vivo</it>, in certain adverse metabolic conditions in which insulin action is precluded. In comparative studies of normal and mutant mice, glucagon administration caused a considerable upregulation of HMGA1 and RBP4 expression both at the mRNA and protein level in wild-type animals. Conversely, in <it>Hmga1</it>-knockout mice, basal and glucagon-mediated expression of RBP4 was severely attenuated and correlated inversely with increased <it>Glut4 </it>mRNA and protein abundance in skeletal muscle and fat, in which the activation state of the protein kinase Akt, an important downstream mediator of the metabolic effects of insulin on Glut4 translocation and carbohydrate metabolism, was simultaneously increased.</p> <p>Conclusion</p> <p>These results indicate that HMGA1 is an important modulator of <it>RBP4 </it>gene expression <it>in vivo</it>. Further, they provide evidence for the identification of a novel biochemical pathway involving the cAMP-HMGA1-RBP4 system, whose activation may play a role in glucose homeostasis in both rodents and humans. Elucidating these mechanisms has importance for both fundamental biology and therapeutic implications.</p

Modelling PCDH19 clustering epilepsy by Neurogenin 2 induction of patient-derived induced pluripotent stem cells

Background: Loss of function mutations in PCDH19 gene causes an X-linked, infant-onset clustering epilepsy, associated with intellectual disability and autistic features. The unique pattern of inheritance includes random X-chromosome inactivation, which leads to pathological tissue mosaicism. Females carrying PCDH19 mutations are affected, while males have a normal phenotype. No cure is presently available for this disease.Methods: Fibroblasts from a female patient carrying frameshift mutation were reprogrammed into human induced pluripotent stem cells (hiPSCs). To create a cell model of PCDH19-clustering epilepsy (PCDH19-CE) where both cell populations co-exist, we created mosaic neurons by mixing wild-type (WT) and mutated (mut) hiPSC clones, and differentiated them into mature neurons with overexpression of the transcriptional factor Neurogenin 2.Results: We generated functional neurons from patient-derived iPSC using a rapid and efficient method of differentiation through overexpression of Neurogenin 2. Was revealed an accelerated maturation and higher arborisation in the mutated neurons, while the mosaic neurons showed the highest frequency of action potential firing and hyperexcitability features, compared to mutated and WT neurons.Conclusions: Our findings provide evidence that PCDH19 c.2133delG mutation affects proper metaphases with increased numbers of centrosomes in stem cells and accelerates neuronal maturation in premature cells. PCDH19 mosaic neurons showed elevated excitability, representing the situation in PCDH19-CE brain. We suggest Ngn2 hiPSC-derived PCDH19 neurons as an informative experimental tool for understanding the pathogenesis of PCDH19-CE and a suitable approach for use in targeted drug screening strategies

LIGHT as regulator of bone homeostasis during osteolytic bone metastasis formation in non-small cell lung cancer patients

Tumor necrosis factor superfamily member 14 (TNFSF14), LIGHT is one of the cytokines produced by tumor and immune cells, which promotes homeostasis of lymphoid organs, liver and bone. Nonsmall cell lung cancer (NSCLC) commonly metastasizes bone, altering bone homeostasis and causing osteolysis. Here we investigated the role of LIGHT in NSCLC-induced osteolytic bone disease. The LIGHT expression in monocytes was higher in patients with metastatic bone lesions than in non-bone metastatic ones (66.5 ± 24.5 vs 43.3 ± 25.2 mean ± SD, p = 0.001), in healthy donors (66.5 ± 24.5 vs 8.5 ± 4.6 p = 0.0002), and in non-bone metastatic patients than in healthy donors (43.3 ± 25.2 vs 8.5 ± 4.6, p = 0.0001). Serum LIGHT levels were also significantly higher in bone metastatic patients than in non-bone metastatic ones (186.8 ± 191.2 pg/ml vs 115.8 ± 73 pg/ml, p = 0.04) and in healthy donors (186.8 ± 191.2 pg/ml vs 85.7 ± 38.4 pg/ml, p = 0.04). A neutralizing mAb anti-LIGHT added to osteoclast (OC) cultures of both bone and non-bone metastases inhibited osteoclastogenesis, but the decrease was statistically significant only for bone metastatic patients (272 ± 98 vs 132 ± 74, p = 0.01). To investigate the role of LIGHT in NSCLC- induced bone lesion in vivo, we performed an intratibial injection of a mouse lung cancer cell line LLC-1, in wild-type (WT) and LIGHT KO mice. The WT-injected mice displayed a significant reduction of about 20% for BV/TV, Tb.N, Tb.Th, and Tb.Sp compared to the WT-vehicle mice (pb 0.01). These parameters did not show significant variation for KO-injected mice vs vehicle or for WT-injected mice vs KO-injected mice. These data indicate LIGHT as a regulator of bone homeostasis during NSCLC metastatic invasion, thus it may be a novel therapeutic target in osteolytic bone metastases