An Improved Tax Scheme for Selfish Routing

We study the problem of routing traffic for independent selfish users in a congested network to minimize the total latency. The inefficiency of selfish routing motivates regulating the flow of the system to lower the total latency of the Nash Equilibrium by economic incentives or penalties. When applying tax to the routes, we follow the definition of [Christodoulou et al, Algorithmica, 2014] to define ePoA as the Nash total cost including tax in the taxed network over the optimal cost in the original network. We propose a simple tax scheme consisting of step functions imposed on the links. The tax scheme can be applied to routing games with parallel links, affine cost functions and single-commodity networks to lower the ePoA to at most 4/3 - epsilon, where epsilon only depends on the discrepancy between the links. We show that there exists a tax scheme in the two link case with an ePoA upperbound less than 1.192 which is almost tight. Moreover, we design another tax scheme that lowers ePoA down to 1.281 for routing games with groups of links such that links in the same group are similar to each other and groups are sufficiently different

Distributed Training Large-Scale Deep Architectures

Scale of data and scale of computation infrastructures together enable the current deep learning renaissance. However, training large-scale deep architectures demands both algorithmic improvement and careful system configuration. In this paper, we focus on employing the system approach to speed up large-scale training. Via lessons learned from our routine benchmarking effort, we first identify bottlenecks and overheads that hinter data parallelism. We then devise guidelines that help practitioners to configure an effective system and fine-tune parameters to achieve desired speedup. Specifically, we develop a procedure for setting minibatch size and choosing computation algorithms. We also derive lemmas for determining the quantity of key components such as the number of GPUs and parameter servers. Experiments and examples show that these guidelines help effectively speed up large-scale deep learning training

Stationary Light Pulses in Cold Atomic Media

Stationary light pulses (SLPs), i.e., light pulses without motion, are formed via the retrieval of stored probe pulses with two counter-propagating coupling fields. We show that there exist non-negligible hybrid Raman excitations in media of cold atoms that prohibit the SLP formation. We experimentally demonstrate a method to suppress these Raman excitations and realize SLPs in laser-cooled atoms. Our work opens the way to SLP studies in cold as well as in stationary atoms and provides a new avenue to low-light-level nonlinear optics.Comment: 4 pages, 4 figure

Functional analysis of BARD1 missense variants in homology-directed repair and damage sensitivity

The BARD1 protein, which heterodimerizes with BRCA1, is encoded by a known breast cancer susceptibility gene. While several BARD1 variants have been identified as pathogenic, many more missense variants exist that do not occur frequently enough to assign a clinical risk. In this paper, whole exome sequencing of over 10,000 cancer samples from 33 cancer types identified from somatic mutations and loss of heterozygosity in tumors 76 potentially cancer-associated BARD1 missense and truncation variants. These variants were tested in a functional assay for homology-directed repair (HDR), as HDR deficiencies have been shown to correlate with clinical pathogenicity for BRCA1 variants. From these 76 variants, 4 in the ankyrin repeat domain and 5 in the BRCT domain were found to be non-functional in HDR. Two known benign variants were found to be functional in HDR, and three known pathogenic variants were non-functional, supporting the notion that the HDR assay can be used to predict the clinical risk of BARD1 variants. The identification of HDR-deficient variants in the ankyrin repeat domain indicates there are DNA repair functions associated with this domain that have not been closely examined. In order to examine whether BARD1-associated loss of HDR function results in DNA damage sensitivity, cells expressing non-functional BARD1 variants were treated with ionizing radiation or cisplatin. These cells were found to be more sensitive to DNA damage, and variations in the residual HDR function of non-functional variants did not correlate with variations in sensitivity. These findings improve the understanding of BARD1 functional domains in DNA repair and support that this functional assay is useful for predicting the cancer association of BARD1 variants.</div