On causality violation in Lyra Geometry

In this paper the causality issues are discussed in a non-Riemannian geometry, called Lyra geometry. It is a non-Riemannian geometry originated from Weyl geometry. In order to compare this geometry with the Riemannian geometry, the Einstein field equations are considered. It is verified that the G\"{o}del and G\"{o}del-type metric are consistent with this non-Riemannian geometry. A non-trivial solution for G\"{o}del universe in the absence of matter sources is determined without analogue in general relativity. Different sources are considered and then different conditions for causal and non-causal solutions are discussed.Comment: 13 pages, accepted for publication in Int. J. Geom. Meth. Mod. Phy

Relic density and CMB constraints on dark matter annihilation with Sommerfeld enhancement

We calculate how the relic density of dark matter particles is altered when their annihilation is enhanced by the Sommerfeld mechanism due to a Yukawa interaction between the annihilating particles. Maintaining a dark matter abundance consistent with current observational bounds requires the normalization of the s-wave annihilation cross section to be decreased compared to a model without enhancement. The level of suppression depends on the specific parameters of the particle model, with the kinetic decoupling temperature having the most effect. We find that the cross section can be reduced by as much as an order of magnitude for extreme cases. We also compute the mu-type distortion of the CMB energy spectrum caused by energy injection from such Sommerfeld-enhanced annihilation. Our results indicate that in the vicinity of resonances, associated with bound states, distortions can be large enough to be excluded by the upper limit |mu|<9.0x10^(-5) found by the COBE/FIRAS experiment.Comment: 10 pages, 6 figures, accepted for publication in Physical Review D. Corrections to eqs. 9,10,14 and 16. Figures updated accordingly. No major changes to previous results. Website with online tools for Sommerfeld-related calculations can be found at http://www.mpa-garching.mpg.de/~vogelsma/sommerfeld

WHAT IS THE LENGTH OF A SNAKE?

The way that herpetologists have traditionally measuredlive snakes is by stretching them on a ruler andrecording the total length (TL). However, due to the thinconstitution of the snake, the large number of intervertebraljoints, and slim muscular mass of most snakes,it is easier to stretch a snake than it is to stretch anyother vertebrate. The result of this is that the length ofa snake recorded is infl uenced by how much the animalis stretched. Stretching it as much as possible is perhapsa precise way to measure the length of the specimenbut it might not correspond to the actual length ofa live animal. Furthermore, it may seriously injure a livesnake. Another method involves placing the snake in aclear plexiglass box and pressing it with a soft materialsuch as rubber foam against a clear surface. Measuringthe length of the snake may be done by outlining itsbody with a string (Fitch 1987; Frye 1991). However, thismethod is restricted to small animals that can be placedin a box, and in addition, no indications of accuracy of thetechnique are given. Measuring the snakes with a fl exibletape has also been reported (Blouin-Demers 2003)but when dealing with a large animals the way the tapeis positioned can produce great variance on the fi nal outcome.In this contribution we revise alternative ways tomeasuring a snake and propose a method that offers repeatableresults. We further analyze the precision of thismethod by using a sample of measurements taken fromwild populations of green anacondas (Eunectes murinus)with a large range of sizes

Novel signaling pathways in pulmonary arterial hypertension (2015 Grover Conference Series)

The proliferative endothelial and smooth muscle cell phenotype, inflammation, and pulmonary vascular remodeling are prominent features of pulmonary arterial hypertension (PAH). Mutations in bone morphogenetic protein type 2 receptor (BMPR2) have been identified as the most common genetic cause of PAH and females with BMPR2 mutations are 2.5 times as likely to develop heritable forms of PAH than males. Higher levels of estrogen have also been observed in males with PAH, implicating sex hormones in PAH pathogenesis. Recently, the estrogen metabolite 16α-OHE1 (hydroxyestrone) was implicated in the regulation of miR29, a microRNA involved in modulating energy metabolism. In females, decreased miR96 enhances serotonin’s effect by upregulating the 5-hydroxytryptamine 1B (5HT1B) receptor. Because PAH is characterized as a quasi-malignant disease, likely due to BMPR2 loss of function, altered signaling pathways that sustain this cancer-like phenotype are being explored. Extracellular signal–regulated kinases 1 and 2 and p38 mitogen-activated protein kinases (MAPKs) play a critical role in proliferation and cell motility, and dysregulated MAPK signaling is observed in various experimental models of PAH. Wnt signaling pathways preserve pulmonary vascular homeostasis, and dysregulation of this pathway could contribute to limited vascular regeneration in response to injury. In this review, we take a closer look at sex, sex hormones, and the interplay between sex hormones and microRNA regulation. We also focus on MAPK and Wnt signaling pathways in the emergence of a proproliferative, antiapoptotic endothelial phenotype, which then orchestrates an angioproliferative process of vascular remodeling, with the hope of developing novel therapies that could reverse the phenotype

Anytime coalition structure generation on synergy graphs

We consider the coalition structure generation (CSG) problem on synergy graphs, which arises in many practical applications where communication constraints, social or trust relationships must be taken into account when forming coalitions. We propose a novel representation of this problem based on the concept of edge contraction, and an innovative branch and bound approach (CFSS), which is particularly efficient when applied to a general class of characteristic functions. This new model provides a non-redundant partition of the search space, hence allowing an effective parallelisation. We evaluate CFSS on two benchmark functions, the edge sum with coordination cost and the collective energy purchasing functions, comparing its performance with the best algorithm for CSG on synergy graphs: DyCE. The latter approach is centralised and cannot be efficiently parallelised due to the exponential memory requirements in the number of agents, which limits its scalability (while CFSS memory requirements are only polynomial). Our results show that, when the graphs are very sparse, CFSS is 4 orders of magnitude faster than DyCE. Moreover, CFSS is the first approach to provide anytime approximate solutions with quality guarantees for very large systems (i.e., with more than 2700 agents

On the Transferability of Knowledge among Vehicle Routing Problems by using Cellular Evolutionary Multitasking

Multitasking optimization is a recently introduced paradigm, focused on the simultaneous solving of multiple optimization problem instances (tasks). The goal of multitasking environments is to dynamically exploit existing complementarities and synergies among tasks, helping each other through the transfer of genetic material. More concretely, Evolutionary Multitasking (EM) regards to the resolution of multitasking scenarios using concepts inherited from Evolutionary Computation. EM approaches such as the well-known Multifactorial Evolutionary Algorithm (MFEA) are lately gaining a notable research momentum when facing with multiple optimization problems. This work is focused on the application of the recently proposed Multifactorial Cellular Genetic Algorithm (MFCGA) to the well-known Capacitated Vehicle Routing Problem (CVRP). In overall, 11 different multitasking setups have been built using 12 datasets. The contribution of this research is twofold. On the one hand, it is the first application of the MFCGA to the Vehicle Routing Problem family of problems. On the other hand, equally interesting is the second contribution, which is focused on the quantitative analysis of the positive genetic transferability among the problem instances. To do that, we provide an empirical demonstration of the synergies arisen between the different optimization tasks.Comment: 8 pages, 1 figure, paper accepted for presentation in the 23rd IEEE International Conference on Intelligent Transportation Systems 2020 (IEEE ITSC 2020

Hypoxia Produces Pro-arrhythmic Late Sodium Current in Cardiac Myocytes by SUMOylation of NaV1.5 Channels.

Acute cardiac hypoxia produces life-threatening elevations in late sodium current (ILATE) in the human heart. Here, we show the underlying mechanism: hypoxia induces rapid SUMOylation of NaV1.5 channels so they reopen when normally inactive, late in the action potential. NaV1.5 is SUMOylated only on lysine 442, and the mutation of that residue, or application of a deSUMOylating enzyme, prevents hypoxic reopenings. The time course of SUMOylation of single channels in response to hypoxia coincides with the increase in ILATE, a reaction that is complete in under 100 s. In human cardiac myocytes derived from pluripotent stem cells, hypoxia-induced ILATE is confirmed to be SUMO-dependent and to produce action potential prolongation, the pro-arrhythmic change observed in patients