Chaotic electron diffusion through stochastic webs enhances current flow in superlattices

Understanding how complex systems respond to change is of fundamental importance in the natural sciences. There is particular interest in systems whose classical newtonian motion becomes chaotic as an applied perturbation grows. The transition to chaos usually occurs by the gradual destruction of stable orbits in parameter space, in accordance with the Kolmogorov-Arnold-Moser (KAM) theorem--a cornerstone of nonlinear dynamics that explains, for example, gaps in the asteroid belt. By contrast, 'non-KAM' chaos switches on and off abruptly at critical values of the perturbation frequency. This type of dynamics has wide-ranging implications in the theory of plasma physics, tokamak fusion, turbulence, ion traps, and quasicrystals. Here we realize non-KAM chaos experimentally by exploiting the quantum properties of electrons in the periodic potential of a semiconductor superlattice with an applied voltage and magnetic field. The onset of chaos at discrete voltages is observed as a large increase in the current flow due to the creation of unbound electron orbits, which propagate through intricate web patterns in phase space. Non-KAM chaos therefore provides a mechanism for controlling the electrical conductivity of a condensed matter device: its extreme sensitivity could find applications in quantum electronics and photonics.     

Selenium: an insulin-mimetic

Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. In recent years, selenium has been shown to mediate a number of insulin-like actions both in vivo and in vitro. These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. The mechanism by which selenium is capable of mimicking insulin is not clear; however, reports indicate that selenium does activate key proteins involved in the insulin-signal cascade. Various proteins in the insulin-signal cascade have been shown to be necessary for different insulin-regulated events, and presumably data will be forthcoming soon that illustrate this similarly for selenium. This review compares the action of selenium to that of insulin and discusses the available evidence in support of selenium as an insulin-mimetic.     

Introduction: the selenium conundrum

Selenium was first suspected of being an essential dietary trace element in the 1950s. We now know that indeed it is an essential biological element that serves as an integral component of several enzymes, including those in the families of deiodinases and glutathione peroxidases as well as selenoproteins P and W. The multi-author review that follows this introduction concentrates on the important biological role of selenium in enzymes as well as some of the physiological aspects of selenium as either a potential anticarcinogenic agent or insulin mimetic. What should become clear from these contributed articles is the complex and dynamic role that selenium plays in many biological processes and that the investigations in these areas are at the edge of exciting new frontiers.     

Positional cloning of Sorcs1, a type 2 diabetes quantitative trait locus

We previously mapped the type 2 diabetes mellitus-2 locus (T2dm2), which affects fasting insulin levels, to distal chromosome 19 in a leptin-deficient obese F2 intercross derived from C57BL/6 (B6) and BTBR T+ tf/J (BTBR) mice. Introgression of a 7-Mb segment of the B6 chromosome 19 into the BTBR background (strain 1339A) replicated the reduced insulin linked to T2dm2. The 1339A mice have markedly impaired insulin secretion in vivo and disrupted islet morphology. We used subcongenic strains derived from 1339A to localize the T2dm2 quantitative trait locus (QTL) to a 242-kb segment comprising the promoter, first exon and most of the first intron of the Sorcs1 gene. This was the only gene in the 1339A strain for which we detected amino acid substitutions and expression level differences between mice carrying B6 and BTBR alleles of this insert, thereby identifying variation within the Sorcs1 gene as underlying the phenotype associated with the T2dm2 locus. SorCS1 binds platelet-derived growth factor, a growth factor crucial for pericyte recruitment to the microvasculature, and may thus have a role in expanding or maintaining the islet vasculature. Our identification of the Sorcs1 gene provides insight into the pathway underlying the pathophysiology of obesity-induced type 2 diabetes mellitus.