A new perspective to rational expectations: maximin rational expectations equilibrium

We introduce a new notion of rational expectations equilibrium (REE) called maximin rational expectations equilibrium (MREE), which is based on the maximin expected utility (MEU) formulation. In particular, agents maximize maximin expected utility conditioned on their own private information and the information that the equilibrium prices generate. Maximin equilibrium allocations need not to be measurable with respect to the private information of each individual and with respect to the information that the equilibrium prices generate, as it is in the case of the Bayesian REE. We prove that a maximin REE exists universally (and not generically as in Radner (1979) and Allen (1981)), it is effcient and incentive compatible. These results are false for the Bayesian REE

Influence of rotational force fields on the determination of the work done on a driven Brownian particle

For a Brownian system the evolution of thermodynamic quantities is a stochastic process. In particular, the work performed on a driven colloidal particle held in an optical trap changes for each realization of the experimental manipulation, even though the manipulation protocol remains unchanged. Nevertheless, the work distribution is governed by established laws. Here, we show how the measurement of the work distribution is influenced by the presence of rotational, i.e. nonconservative, radiation forces. Experiments on particles of different materials show that the rotational radiation forces, and therefore their effect on the work distributions, increase with the particle refractive index.Comment: 12 pages, 4 figure

Formation and evolution of clumpy tidal tails around globular clusters

We present some results of numerical simulations of a globular cluster orbiting in the central region of a triaxial galaxy on a set of 'loop' orbits. Tails start forming after about a quarter of the globular cluster orbital period and develop, in most cases, along the cluster orbit, showing clumpy substructures as observed, for example, in Palomar 5. If completely detectable, clumps can contain about 7,000 solar masses each, i.e. about 10% of the cluster mass at that epoch. The morphology of tails and clumps and the kinematical properties of stars in the tails are studied and compared with available observational data. Our finding is that the stellar velocity dispersion tends to level off at large radii, in agreement to that found for M15 and Omega Centauri.Comment: LaTeX 2e, uses AASTeX v5.x, 40 pages with 18 figures. Submitted to The Astronomical Journa

On the Limit Points of an Infinitely Repeated Rational Expectations Equilibrium

We show that a symmetric information Rational Expectations Equilibrium (REE) exists universally (and not generically), it is Pareto efficient and obviously incentive compatible. Agents, in a repeated economy framework, can reach a symmetric information REE (i.e., an efficient and incentive compatible equilibrium outcome) by observing the past asymmetric REE and also by updating their private information. We also prove the converse result, i.e., given a symmetric information REE, we can construct a sequence of approximate asymmetric REE allocations that converges to the symmetric information REE. The approximate REE can be interpreted as the mistakes that agents make due to bounded rationality, nonetheless, in the limit an exact symmetric information REE is reached. In view of the above results, the symmetric information REE provides a rationalization for the asymmetric one

Diabetes and pancreatic cancer-a dangerous liaison relying on carbonyl stress

Both type 2 (T2DM) and type 1 (T1DM) diabetes mellitus confer an increased risk of pancreatic cancer in humans. The magnitude and temporal trajectory of the risk conferred by the two forms of diabetes are similar, suggesting a common mechanism. Carbonyl stress is a hallmark of hyperglycemia and dyslipidemia, which accompanies T2DM, prediabetes, and obesity. Accumulating evidence demonstrates that diabetes promotes pancreatic ductal adenocarcinoma (PDAC) in experimental models of T2DM, a finding recently confirmed in a T1DM model. The carbonyl stress markers advanced glycation end-products (AGEs), the levels of which are increased in diabetes, were shown to markedly accelerate tumor development in a mouse model of Kras-driven PDAC. Consistently, inhibition of AGE formation by trapping their carbonyl precursors (i.e., reactive carbonyl species, RCS) prevented the PDAC-promoting effect of diabetes. Considering the growing attention on carbonyl stress in the onset and progression of several cancers, including breast, lung and colorectal cancer, this review discusses the mechanisms by which glucose and lipid imbalances induce a status of carbonyl stress, the oncogenic pathways activated by AGEs and their precursors RCS, and the potential use of carbonyl-scavenging agents and AGE inhibitors in PDAC prevention and treatment, particularly in high-risk diabetic individuals

Diabetic complications and oxidative stress: A 20‐year voyage back in time and back to the future

Twenty years have passed since Brownlee and colleagues proposed a single unifying mechanism for diabetic complications, introducing a turning point in this field of research. For the first time, reactive oxygen species (ROS) were identified as the causal link between hyperglycemia and four seemingly independent pathways that are involved in the pathogenesis of diabetes-associated vascular disease. Before and after this milestone in diabetes research, hundreds of articles describe a role for ROS, but the failure of clinical trials to demonstrate antioxidant benefits and some recent experimental studies showing that ROS are dispensable for the pathogenesis of diabetic complications call for time to reflect. This twenty‐year journey focuses on the most relevant literature regarding the main sources of ROS generation in diabetes and their role in the pathogenesis of cell dysfunction and diabetic complications. To identify future research directions, this review discusses the evidence in favor and against oxidative stress as an initial event in the cellular biochemical abnormalities induced by hyperglycemia. It also explores possible alternative mechanisms, including carbonyl stress and the Warburg effect, linking glucose and lipid excess, mitochondrial dysfunction, and the activation of alternative pathways of glucose metabolism leading to vascular cell injury and inflammation