ALTERNATIVE AUCTION INSTITUTIONS FOR ELECTRIC POWER MARKETS

Restructuring of electric power markets is proceeding across the United States and in many other nations around the world. The performance of these markets will influence everything from the prices faced by consumers to the reliability of the systems. The challenges of these changes present many important areas for research. For much of the northeastern United States, restructuring proposals include, at least for the short term, the formation of a single-sided auction mechanism for the wholesale market. This research uses experimental methods to analyze how these markets may function. In the experiments, the two basic uniform price auction rules are tested under three different market sizes. Early experimental results suggest the commonly proposed last-accepted-offer auction works well, but market power could be a real concern.Resource /Energy Economics and Policy,

Towards a multidimensional healthy ageing phenotype

Purpose of review: There is great interest in developing tools to measure healthy ageing and to identify early stages of health impairment, which may guide the implementation of interventions to prevent or delay the development of disease, disability, and mortality. Here, we review the most recent developments directed to operationalize, and test, definitions of healthy ageing. Recent findings: There is lack of consensus about how to define healthy ageing and, unsurprisingly, diversity in the instruments for its measurement. However, progress is being made in describing and in devising tools to capture the healthy ageing phenotype. Attempts to measure healthy ageing have relied primarily on cross-sectional data collected in older people. More recent studies have assessed the healthy ageing phenotype using markers of multiple functional domains and have used longitudinal data to model the dynamics and trajectories of healthy ageing. Summary: Given the complexity of the ageing process, no single measure is able to predict the ageing trajectory. Current attempts to operationalize the healthy ageing phenotype have relied on markers and data from earlier cohort studies and are limited by the tools used to collect data in those studies. Such data are often unsuitable to detect early subtle declines in function and/or are inappropriate for use in younger old adults. Future studies employing more objective and novel markers of healthy ageing are likely to offer opportunities to define and operationalize the healthy ageing phenotype

Ergodic Theory for Interested Computer Scientists

Abstract We describe ergodic theory in modern notation accessible to interested computer scientists. The ergodic theorem (http://en.wikipedia.org/wiki/Ergodic theory (link)) is an important principle of recurrence and averaging in dynamical systems. However, there are some inconsistent uses of the term, much of the machinery is intended to work with deterministic dynamical systems (not probabilistic systems, as is often implied) and often the conclusion of the theory is mis-described as its premises

TAMESIS (Río). Mapas hidrográficos (1767). 1:105000

Fecha de publicación tomada de "Tooley's dictionary of Mapmakers", Tring, 1979, p. 166Escala gráfica de 10 millas [= 15,4 cm]. Orientado con lis en rosa de treinta y dos vientos prolongadosOrografía de perfil. Indica sondas batimétricas y bancos de arenaEn el margen inferior una tabla refleja los bancos, estrechos que tiene el río y una amplia leyenda informa cómo navegar por élTítulo enmarcado en cartela decorada con motivos alegóricos y vegetale

The letters of John Ruskin to Lord and Lady Mount-Temple

(print) xiii, 399 p. ; 24 cmIntroduction 5 -- Part I : [1856]-February 10, 1866 15 -- Part II : [February 1866]-June 25, 1867 55 -- Part III : 1868 121 -- Part IV : January 17, 1869-[July 27, 1871] 185 -- Part V : July 27, 1871-May 30, [1888] 301 -- Appendix : Publishing History of the Letters 387 -- Index 59

SplicePort—An interactive splice-site analysis tool

SplicePort is a web-based tool for splice-site analysis that allows the user to make splice-site predictions for submitted sequences. In addition, the user can also browse the rich catalog of features that underlies these predictions, and which we have found capable of providing high classification accuracy on human splice sites. Feature selection is optimized for human splice sites, but the selected features are likely to be predictive for other mammals as well. With our interactive feature browsing and visualization tool, the user can view and explore subsets of features used in splice-site prediction (either the features that account for the classification of a specific input sequence or the complete collection of features). Selected feature sets can be searched, ranked or displayed easily. The user can group features into clusters and frequency plot WebLogos can be generated for each cluster. The user can browse the identified clusters and their contributing elements, looking for new interesting signals, or can validate previously observed signals. The SplicePort web server can be accessed at http://www.cs.umd.edu/projects/SplicePort and http://www.spliceport.org

Insulin-stimulated phosphorylation of endothelial nitric oxide synthase at serine-615 contributes to nitric oxide synthesis

Insulin stimulates endothelial NO (nitric oxide) synthesis via PKB (protein kinase B)/Akt-mediated phosphorylation and activation of eNOS (endothelial NO synthase) at Ser-1177. In previous studies, we have demonstrated that stimulation of eNOS phosphorylation at Ser-1177 may be required, yet is not sufficient for insulin-stimulated NO synthesis. We therefore investigated the role of phosphorylation of eNOS at alternative sites to Ser-1177 as candidate parallel mechanisms contributing to insulin-stimulated NO synthesis. Stimulation of human aortic endothelial cells with insulin rapidly stimulated phosphorylation of both Ser-615 and Ser-1177 on eNOS, whereas phosphorylation of Ser-114, Thr-495 and Ser-633 was unaffected. Insulin-stimulated Ser-615 phosphorylation was abrogated by incubation with the PI3K (phosphoinositide 3-kinase) inhibitor wortmannin, infection with adenoviruses expressing a dominant-negative mutant PKB/Akt or pre-incubation with TNFα (tumour necrosis factor α), but was unaffected by high culture glucose concentrations. Mutation of Ser-615 to alanine reduced insulin-stimulated NO synthesis, whereas mutation of Ser-615 to aspartic acid increased NO production by NOS in which Ser-1177 had been mutated to an aspartic acid residue. We propose that the rapid PKB-mediated stimulation of phosphorylation of Ser-615 contributes to insulin-stimulated NO synthesis

Insights from GWAS: emerging landscape of mechanisms underlying complex trait disease

There are now over 2000 loci in the human genome where genome wide association studies (GWAS) have found one or more SNPs to be associated with altered risk of a complex trait disease. At each of these loci, there must be some molecular level mechanism relevant to the disease. What are these mechanisms and how do they contribute to disease? Here we consider the roles of three primary mechanism classes: changes that directly alter protein function (missense SNPs), changes that alter transcript abundance as a consequence of variants close-by in sequence, and changes that affect splicing. Missense SNPs are divided into those predicted to have a high impact on in vivo protein function, and those with a low impact. Splicing is divided into SNPs with a direct impact on splice sites, and those with a predicted effect on auxiliary splicing signals. The analysis was based on associations found for seven complex trait diseases in the classic Wellcome Trust Case Control Consortium (WTCCC1) GWA study and subsequent studies and meta-analyses, collected from the GWAS catalog. Linkage disequilibrium information was used to identify possible candidate SNPs for involvement in disease mechanism in each of the 356 loci associated with these seven diseases. With the parameters used, we find that 76% of loci have at least of these mechanisms. Overall, except for the low incidence of direct impact on splice sites, the mechanisms are found at similar frequencies, with changes in transcript abundance the most common. But the distribution of mechanisms over diseases varies markedly, as does the fraction of loci with assigned mechanisms. Many of the implicated proteins have previously been suggested as relevant, but the specific mechanism assignments are new. In addition, a number of new disease relevant proteins are proposed. The high fraction of GWAS loci with proposed mechanisms suggests that these classes of mechanism play a major role. Other mechanism types, such as variants affecting expression of genes remote in the DNA sequence, will contribute in other loci. Each of the identified putative mechanisms provides a hypothesis for further investigation.https://doi.org/10.1186/1471-2164-16-S8-S