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We provide mechanisms and new metric distortion bounds for line-up elections. In such elections, a set of n voters, k candidates, and ell positions are all located in a metric space. The goal is to choose a set of candidates and assign them to different positions, so as to minimize the total cost of the voters. The cost of each voter consists of the distances from itself to the chosen candidates (measuring how much the voter likes the chosen candidates, or how similar it is to them), as well as the distances from the candidates to the positions they are assigned to (measuring the fitness of the candidates for their positions). Our mechanisms, however, do not know the exact distances, and instead produce good outcomes while only using a smaller amount of information, resulting in small distortion.We consider several different types of information: ordinal voter preferences, ordinal position preferences, and knowing the exact locations of candidates and positions, but not those of voters. In each of these cases, we provide constant distortion bounds, thus showing that only a small amount of information is enough to form outcomes close to optimum in line-up elections. 

Vascular endothelial cells (ECs) sense and respond to hemodynamic forces such as pulsatile shear stress (PS) and oscillatory shear stress (OS). Among the metabolic pathways, glycolysis is differentially regulated by atheroprone OS and atheroprotective PS. Studying the molecular mechanisms by which PS suppresses glycolytic flux at the epigenetic, transcriptomic, and kinomic levels, we have demonstrated that glucokinase regulatory protein (GCKR) was markedly induced by PS in vitro and in vivo, although PS down-regulates other glycolysis enzymes such as hexokinase (HK1). Using next-generation sequencing data, we identified the binding of PS-induced Krüppel-like factor 4 (KLF4), which functions as a pioneer transcription factor, binding to the GCKR promoter to change the chromatin structure for transactivation of GCKR. At the posttranslational level, PS-activated AMP-activated protein kinase (AMPK) phosphorylates GCKR at Ser-481, thereby enhancing the interaction between GCKR and HK1 in ECs. In vivo, the level of phosphorylated GCKR Ser-481 and the interaction between GCKR and HK1 were increased in the thoracic aorta of wild-type AMPKα2^+/+mice in comparison with littermates with EC ablation of AMPKα2 (AMPKα2^−/−). In addition, the level of GCKR was elevated in the aortas of mice with a high level of voluntary wheel running. The underlying mechanisms for the PS induction of GCKR involve regulation at the epigenetic level by KLF4 and at the posttranslational level by AMPK. 

A key issue, whenever people work together to solve a complex problem, is how to divide the problem into parts done by different people and combine the parts into a solution for the whole problem. This paper presents a novel way of doing this with groups of contests called contest webs. Based on the analogy of supply chains for physical products, the method provides incentives for people to (a) reuse work done by themselves and others, (b) simultaneously explore multiple ways of combining interchangeable parts, and (c) work on parts of the problem where they can contribute the most. The paper also describes a field test of this method in an online community of over 50,000 people who are developing proposals for what to do about global climate change. The early results suggest that the method can, indeed, work at scale as intended.