Analysis of Vector-Inflation Models Using Dynamical Systems

We analyze two possible vector-field models using the techniques of dynamical systems. The first model involves a U(1)-vector field and the second a triad of SU(2)-vector fields. Both models include a gauge-fixing term and a power-law potential. A dynamical system is formulated and it is found that one of the critical points, for each model, corresponds to inflation, the origin of these critical points being the respective gauge-fixing terms. The conditions for the existence of an inflationary era which lasts for at least 60 efolds are studied.Comment: LaTeX file in elsarticle style, 4 pages, 1 figure. To be published in Nuclear Physics B Proceedings Supplement as the proceedings of the Tenth Latin American Symposium on High Energy Physics (Medellin - Colombia, 24th-28th November, 2014

New Non-Abelian Reissner-Nordstr\"{o}m Black Hole Solutions in the Generalized SU(2) Proca Theory And Some Astrophysical Implications

The Generalized SU(2) Proca theory is a vector-tensor theory of gravity whose action is invariant under global transformations of the SU(2) group and includes second-order derivative self-interactions of the vector field beyond the massive Yang-Mills theory. We find that the presence of two Lagrangian pieces consisting of four gauge fields minimally coupled to gravity gives rise to an exact Reissner-Nordstr\"{o}m black hole solution endowed with two different non-Abelian effective charges that depend on the specific combination, $\chi = 2\chi_1 + \chi_2$, of the respective coupling constants. After studying the spacetime structure of the black hole, some astrophysical implications of the black hole solutions are investigated. First, joint analysis of observations of the EHT's first images of Sagittarius A$^{\star}$ of our Galaxy set the first serious constraint on the free parameters of the theory beyond the theoretical bounds found. Second, we investigate the accretion properties of spherical steady flows around this class of non-Abelian Reissner-Nordstr\"{o}m black hole. Specifically, we examine the general conditions under which transonic flow is allowed. Analytical solution for critical accretion is found in terms of the coupling constant. In addition, we explore numerically the effect of changing $\chi$ on the radial velocity and mass density, and show how the extremal Reissner-Nordstr\"{o}m and the standard Schwarzschild solutions as limit cases are achieved. Lastly, working in the fully relativistic regime, an analytical expression for the critical mass accretion rate of a polytropic fluid onto a black hole is derived. As a main result, we find that the critical accretion rate efficiency can be noticeably improved compared to the Schwarzschild case for a specific region of the parameter space where the non-Abelian charge becomes imaginary.Comment: 17 pages, 8 figure

The mechanisms of potassium loss in acute myocardial ischemia: New insights from computational simulations

: Acute myocardial ischemia induces hyperkalemia (accumulation of extracellular potassium), a major perpetrator of lethal reentrant ventricular arrhythmias. Despite considerable experimental efforts to explain this pathology in the last decades, the intimate mechanisms behind hyperkalemia remain partially unknown. In order to investigate these mechanisms, we developed a novel computational model of acute myocardial ischemia which couples a) an electrophysiologically detailed human cardiomyocyte model that incorporates modifications to account for ischemia-induced changes in transmembrane currents, with b) a model of cardiac tissue and extracellular K + transport. The resulting model is able to reproduce and explain the triphasic time course of extracellular K + concentration within the ischemic zone, with values of [K+]o close to 14 mmol/L in the central ischemic zone after 30 min. In addition, the formation of a [K+]o border zone of approximately 1.2 cm 15 min after the onset of ischemia is predicted by the model. Our results indicate that the primary rising phase of [K+]o is mainly due to the imbalance between K + efflux, that increases slightly, and K + influx, that follows a reduction of the NaK pump activity by more than 50%. The onset of the plateau phase is caused by the appearance of electrical alternans (a novel mechanism identified by the model), which cause an abrupt reduction in the K + efflux. After the plateau, the secondary rising phase of [K+]o is caused by a subsequent imbalance between the K + influx, which continues to decrease slowly, and the K + efflux, which remains almost constant. Further, the study shows that the modulation of these mechanisms by the electrotonic coupling is the main responsible for the formation of the ischemic border zone in tissue, with K + transport playing only a minor role. Finally, the results of the model indicate that the injury current established between the healthy and the altered tissue is not sufficient to depolarize non-ischemic cells within the healthy tissue

Loss of Mitochondrial Membrane Potential Triggers the Retrograde Response Extending Yeast Replicative Lifespan

In the budding yeast Saccharomyces cerevisiae, loss of mitochondrial DNA (rho0) can induce the retrograde response under appropriate conditions, resulting in increased replicative lifespan (RLS). Although the retrograde pathway has been extensively elaborated, the nature of the mitochondrial signal triggering this response has not been clear. Mitochondrial membrane potential (MMP) was severely reduced in rho0 compared to rho+ cells, and RLS was concomitantly extended. To examine the role of MMP in the retrograde response, MMP was increased in the rho0 strain by introducing a mutation in the ATP1 gene, and it was decreased in rho+ cells by deletion of COX4. The ATP1-111 mutation in rho0 cells partially restored the MMP and reduced mean RLS to that of rho+ cells. COX4 deletion decreased MMP in rho+ cells to a value intermediate between rho+ and rho0 cells and similarly increased RLS. The increase in expression of CIT2, the diagnostic gene for the retrograde response, seen in rho0 cells, was substantially suppressed in the presence of the ATP1-111 mutation. In contrast, CIT2 expression increased in rho+ cells on deletion of COX4. Activation of the retrograde response results in the translocation of the transcription factor Rtg3 from the cytoplasm to the nucleus. Rtg3–GFP translocation to the nucleus was directly observed in rho0 and rho+ cox4Δ cells, but it was blunted in rho0 cells with the ATP1-111 mutation. We conclude that a decrease in MMP is the signal that initiates the retrograde response and leads to increased RLS