Cost-sharing in generalised selfish routing

© Springer International Publishing AG 2017. We study a generalisation of atomic selfish routing games where each player may control multiple flows which she routes seek-ing to minimise their aggregate cost. Such games emerge in various set-tings, such as traffic routing in road networks by competing ride-sharing applications or packet routing in communication networks by competing service providers who seek to optimise the quality of service of their cus-tomers. We study the existence of pure Nash equilibria in the induced games and we exhibit a separation from the single-commodity per player model by proving that the Shapley value is the only cost-sharing method that guarantees it. We also prove that the price of anarchy and price of stability is no larger than in the single-commodity model for general cost-sharing methods and general classes of convex cost functions. We close by giving results on the existence of pure Nash equilibria of a splittable variant of our model

Recognition of affect in the wild using deep neural networks

In this paper we utilize the first large-scale "in-the-wild" (Aff-Wild) database, which is annotated in terms of the valence-arousal dimensions, to train and test an end-to-end deep neural architecture for the estimation of continuous emotion dimensions based on visual cues. The proposed architecture is based on jointly training convolutional (CNN) and recurrent neural network (RNN) layers, thus exploiting both the invariant properties of convolutional features, while also modelling temporal dynamics that arise in human behaviour via the recurrent layers. Various pre-trained networks are used as starting structures which are subsequently appropriately fine-tuned to the Aff-Wild database. Obtained results show premise for the utilization of deep architectures for the visual analysis of human behaviour in terms of continuous emotion dimensions and analysis of different types of affect

Universal Programmable Quantum Circuit Schemes to Emulate an Operator

Unlike fixed designs, programmable circuit designs support an infinite number of operators. The functionality of a programmable circuit can be altered by simply changing the angle values of the rotation gates in the circuit. Here, we present a new quantum circuit design technique resulting in two general programmable circuit schemes. The circuit schemes can be used to simulate any given operator by setting the angle values in the circuit. This provides a fixed circuit design whose angles are determined from the elements of the given matrix-which can be non-unitary-in an efficient way. We also give both the classical and quantum complexity analysis for these circuits and show that the circuits require a few classical computations. They have almost the same quantum complexities as non-general circuits. Since the presented circuit designs are independent from the matrix decomposition techniques and the global optimization processes used to find quantum circuits for a given operator, high accuracy simulations can be done for the unitary propagators of molecular Hamiltonians on quantum computers. As an example, we show how to build the circuit design for the hydrogen molecule.Comment: combined with former arXiv:1207.174

A Splicing Mutation in the Novel Mitochondrial Protein DNAJC11 Causes Motor Neuron Pathology Associated with Cristae Disorganization, and Lymphoid Abnormalities in Mice

Mitochondrial structure and function is emerging as a major contributor to neuromuscular disease, highlighting the need for the complete elucidation of the underlying molecular and pathophysiological mechanisms. Following a forward genetics approach with N-ethyl-N-nitrosourea (ENU)-mediated random mutagenesis, we identified a novel mouse model of autosomal recessive neuromuscular disease caused by a splice-site hypomorphic mutation in a novel gene of unknown function, DnaJC11. Recent findings have demonstrated that DNAJC11 protein co-immunoprecipitates with proteins of the mitochondrial contact site (MICOS) complex involved in the formation of mitochondrial cristae and cristae junctions. Homozygous mutant mice developed locomotion defects, muscle weakness, spasticity, limb tremor, leucopenia, thymic and splenic hypoplasia, general wasting and early lethality. Neuropathological analysis showed severe vacuolation of the motor neurons in the spinal cord, originating from dilatations of the endoplasmic reticulum and notably from mitochondria that had lost their proper inner membrane organization. The causal role of the identified mutation in DnaJC11 was verified in rescue experiments by overexpressing the human ortholog. The full length 63 kDa isoform of human DNAJC11 was shown to localize in the periphery of the mitochondrial outer membrane whereas putative additional isoforms displayed differential submitochondrial localization. Moreover, we showed that DNAJC11 is assembled in a high molecular weight complex, similarly to mitofilin and that downregulation of mitofilin or SAM50 affected the levels of DNAJC11 in HeLa cells. Our findings provide the first mouse mutant for a putative MICOS protein and establish a link between DNAJC11 and neuromuscular diseases

Aff-Wild: Valence and Arousal ‘in-the-wild’ Challenge

The Affect-in-the-Wild (Aff-Wild) Challenge proposes a new comprehensive benchmark for assessing the performance of facial affect/behaviour analysis/understanding 'in-the-wild'. The Aff-wild benchmark contains about 300 videos (over 2,000 minutes of data) annotated with regards to valence and arousal, all captured 'in-the-wild' (the main source being Youtube videos). The paper presents the database description, the experimental set up, the baseline method used for the Challenge and finally the summary of the performance of the different methods submitted to the Affect-in-the-Wild Challenge for Valence and Arousal estimation. The challenge demonstrates that meticulously designed deep neural networks can achieve very good performance when trained with in-the-wild data

Regulated expression of human A γ-, β-, and hybrid γ β-globin genes in transgenic mice: manipulation of the developmental expression patterns.

We have introduced the human fetal gamma- and adult beta-globin genes into the germ line of mice. Analysis of the resulting transgenic mice shows that the human gamma-globin gene is expressed like an embryonic mouse globin gene; the human beta-globin gene is expressed (as previously shown) like an adult mouse globin gene. These results imply that the regulatory signals for tissue- and developmental stage-specific expression of the globin genes have been conserved between man and mouse but that the timing of the signals has changed. Because the two genes are expressed differently, we introduced a hybrid gamma beta-globin gene construct. The combination of the regulatory sequences resulted in the expression of the hybrid gene at all stages in all the murine erythroid tissues

T-cell independent Thy-1 allo-antibody response with the use of transgenic mice.

We have introduced a mouse Thy-1.1 gene into the germline of Thy-1.2 mice. The introduced gene was shown to be expressed at very high levels in thymocytes when compared with the endogenous gene. Transgenic thymocytes were shown to evoke a higher than normal primary anti-Thy-1.1 antibody response in plaque-forming cell (PFC) assays. This result suggests that a direct quantitative interaction of the Thy-1 antigen activates the B cell response