Towards Machine Wald

The past century has seen a steady increase in the need of estimating and predicting complex systems and making (possibly critical) decisions with limited information. Although computers have made possible the numerical evaluation of sophisticated statistical models, these models are still designed \emph{by humans} because there is currently no known recipe or algorithm for dividing the design of a statistical model into a sequence of arithmetic operations. Indeed enabling computers to \emph{think} as \emph{humans} have the ability to do when faced with uncertainty is challenging in several major ways: (1) Finding optimal statistical models remains to be formulated as a well posed problem when information on the system of interest is incomplete and comes in the form of a complex combination of sample data, partial knowledge of constitutive relations and a limited description of the distribution of input random variables. (2) The space of admissible scenarios along with the space of relevant information, assumptions, and/or beliefs, tend to be infinite dimensional, whereas calculus on a computer is necessarily discrete and finite. With this purpose, this paper explores the foundations of a rigorous framework for the scientific computation of optimal statistical estimators/models and reviews their connections with Decision Theory, Machine Learning, Bayesian Inference, Stochastic Optimization, Robust Optimization, Optimal Uncertainty Quantification and Information Based Complexity.Comment: 37 page

Electra IRP voltage control strategy for enhancing power system stability in future grid architectures

This study is intended to show the future voltage control strategy designed in the framework of the ELECTRA Integrated Research Programme (IRP) project for the web-of-cells (WoC) concept. This scheme, called post-primary voltage control, aims to keep the node voltages at any time within the bands defined by the regulations and to minimise the power losses in the system by calculating the optimal voltage set-points for the different nodes. The reactive power will mainly be used to restore the voltages but also active power could be delivered in some cells depending on their voltage levels. Different operating modes of the voltage control will be discussed taking both planning and the real-time operation phases into account. The application of the voltage control strategy to one test grid considered as representative of the WoC structure will also be shown in this study.The research leading to these results has received funding from the European Union Seventh Framework Programme (FP7/2007– 2013) under grant agreement no. 609687

Totopotomoy [1864]

Scale 1:21,120.LC Civil War Maps (2nd ed.), 663.2In this issue, the map is printed on a yellow background with the Pamunkey River colored green.Detailed map giving Union works in blue and Confederate works in red, roads, "Virginia Central R.R.," houses, names of residents, vegetation, drainage, and relief by hachures.Description derived from published bibliography

Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming.

A current paradigm proposes that mitochondrial damage is a critical determinant of NLRP3 inflammasome activation. Here, we genetically assess whether mitochondrial signalling represents a unified mechanism to explain how NLRP3 is activated by divergent stimuli. Neither co-deletion of the essential executioners of mitochondrial apoptosis BAK and BAX, nor removal of the mitochondrial permeability transition pore component cyclophilin D, nor loss of the mitophagy regulator Parkin, nor deficiency in MAVS affects NLRP3 inflammasome function. In contrast, caspase-8, a caspase essential for death-receptor-mediated apoptosis, is required for efficient Toll-like-receptor-induced inflammasome priming and cytokine production. Collectively, these results demonstrate that mitochondrial apoptosis is not required for NLRP3 activation, and highlight an important non-apoptotic role for caspase-8 in regulating inflammasome activation and pro-inflammatory cytokine levels