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We construct Cournot games with limited demand, resulting into capped sales volumes according to the respective production shares of the players. We show that such games admit three distinct equilibrium regimes, including an intermediate regime that allows for a range of possible equilibria. When information on demand is modeled by a delayed diffusion process, we also show that this intermediate regime collapses to a single equilibrium while the other regimes approximate the deterministic setting as the delay tends to zero. Moreover, as the delay approaches zero, the unique equilibrium achieved in the stochastic case provides a way to select a natural equilibrium within the range observed in the no lag setting. Numerical illustrations are presented when demand is modeled by an Ornstein–Uhlenbeck process and price is an affine function of output.

The incentive ratio measures the utility gains from strategic behaviour. Without any restrictions on the setup, ratios for linear, Leontief and Cobb-Douglas exchange markets are unbounded, showing that manipulating the equilibrium is a worthwhile endeavour, even if it is computationally challenging. Such unbounded improvements can be achieved even if agents only misreport their utility functions. This provides a sharp contrast with previous results from Fisher markets. When the Cobb-Douglas setup is more restrictive, the maximum utility gain is bounded by the number of commodities. By means of an example, we show that it is possible to exceed a known upper bound for Fisher markets in exchange economies.

This paper introduces a class of games called the positive semidefinite games, for which we show the absence of mixed and nonstrict ESS's. As a result, a strategy is an ESS if and only if it is strict Nash. One famous example in this class of games is Rock{Paper{Scissors. For a smaller class of games called the positive definite games, we prove a similar result forThis paper introduces a class of games called the positive semidefinite games, for which we show the absence of mixed and nonstrict ESS's. As a result, a strategy is an ESS if and only if it is strict Nash. One famous example in this class of games is Rock{Paper{Scissors. For a smaller class of games called the positive definite games, we prove a similar result for NSS's. This result opens the door to a corollary: for doubly symmetric games, the existence of an ESS is assured. This is an interesting result because of the stronger dynamic stability properties of ESS's as compared to NSS's. The coordination games played on the identity matrix are an example of games in this latter class. NSS's. This result opens the door to a corollary: for doubly symmetricgames, the existence of an ESS is assured. This is an interesting result because of the stronger dynamic stability properties of ESS's as compared to NSS's. The coordination games played on the identity matrix are anexample of games in this latter class.

Partial gain of chromosome arm 17q is an abundant aberrancy in various cancer types such as lung and prostate cancer with a prominent occurrence and prognostic significance in neuroblastoma--one of the most common embryonic tumors. The specific genetic element/s in 17q responsible for the cancer-promoting effect of these aberrancies is yet to be defined although many genes located in 17q have been proposed to play a role in malignancy. We report here the characterization of a naturally-occurring, non-reciprocal translocation der(X)t(X;17) in human lung embryonal-derived cells following continuous culturing. This aberrancy was strongly correlated with an increased proliferative capacity and with an acquired ability to form colonies in vitro. The breakpoint region was mapped by fluorescence in situ hybridization (FISH) to the 17q24.3 locus. Further characterization by a custom-made comparative genome hybridization array (CGH) localized the breakpoint within the Bromodomain PHD finger Transcription Factor gene (BPTF), a gene involved in transcriptional regulation and chromatin remodeling. Interestingly, this translocation led to elevation in the mRNA levels of the endogenous BPTF. Knock-down of BPTF restricted proliferation suggesting a role for BPTF in promoting cellular growth. Furthermore, the BPTF chromosomal region was found to be amplified in various human tumors, especially in neuroblastomas and lung cancers in which 55% and 27% of the samples showed gain of 17q24.3, respectively. Additionally, 42% percent of the cancer cell lines comprising the NCI-60 had an abnormal BPTF locus copy number. We suggest that deregulation of BPTF resulting from the translocation may confer the cells with the observed cancer-promoting phenotype and that our cellular model can serve to establish causality between 17q aberrations and carcinogenesis.