Cosmological dynamics of tachyonic teleparallel dark energy

A detailed dynamical analysis of the tachyonic teleparallel dark energy model, in which a non-canonical scalar field (tachyon field) is non-minimally coupled to gravitation, is performed. It is found that, when the non-minimal coupling is ruled by a dynamically changing coefficient $\alpha\equiv f_{,\phi}/\sqrt{f}$, with $f(\phi)$ an arbitrary function of the scalar field $\phi$, the universe may experience a field-matter-dominated era "$\phi$MDE", in which it has some portions of the energy density of $\phi$ in the matter dominated era. This is the most significant difference in relation to the so-called teleparallel dark energy scenario, in which a canonical scalar field (quintessence) is non-minimally coupled to gravitation.Comment: 14 pages, 1 figure. arXiv admin note: text overlap with arXiv:1305.047

Violation of causality in f(T)f(T) gravity

[Abridged] In its standard formulation, the $f(T)$ field equations are not invariant under local Lorentz transformations, and thus the theory does not inherit the causal structure of special relativity. A locally Lorentz covariant $f(T)$ gravity theory has been devised recently, and this local causality problem has been overcome. The nonlocal question, however, is left open. If gravitation is to be described by this covariant $f(T)$ gravity theory there are a number of issues that ought to be examined in its context, including the question as to whether its field equations allow homogeneous G\"odel-type solutions, which necessarily leads to violation of causality on nonlocal scale. Here, to look into the potentialities and difficulties of the covariant $f(T)$ theories, we examine whether they admit G\"odel-type solutions. We take a combination of a perfect fluid with electromagnetic plus a scalar field as source, and determine a general G\"odel-type solution, which contains special solutions in which the essential parameter of G\"odel-type geometries, $m^2$, defines any class of homogeneous G\"odel-type geometries. We extended to the context of covariant $f(T)$ gravity a theorem, which ensures that any perfect-fluid homogeneous G\"odel-type solution defines the same set of G\"odel tetrads $h_A^{~\mu}$ up to a Lorentz transformation. We also shown that the single massless scalar field generates G\"odel-type solution with no closed timelike curves. Even though the covariant $f(T)$ gravity restores Lorentz covariance of the field equations and the local validity of the causality principle, the bare existence of the G\"odel-type solutions makes apparent that the covariant formulation of $f(T)$ gravity does not preclude non-local violation of causality in the form of closed timelike curves.Comment: 10 pages, V2: Presentation of Sec.2 improved, references added, version published in Eur.Phys.J.

Conformal and gauge invariant spin-2 field equations

Using an approach based on the Casimir operators of the de Sitter group, the conformal invariant equations for a fundamental spin-2 field are obtained, and their consistency discussed. It is shown that, only when the spin-2 field is interpreted as a 1-form assuming values in the Lie algebra of the translation group, rather than a symmetric second-rank tensor, the field equation is both conformal and gauge invariant.Comment: 12 pages, no figures; accepted for publication in Gravitation & Cosmolog

Downregulation of BK channel expression in the pilocarpine model of temporal lobe epilepsy

In the hippocampus, BK channels are preferentially localized in presynaptic glutamatergic terminals including mossy fibers where they are thought to play an important role regulating excessive glutamate release during hyperactive states. Large conductance calcium-activated potassium channels (BK, MaxiK, Slo) have recently been implicated in the pathogenesis of genetic epilepsy. However, the role of BK channels in acquired mesial temporal lobe epilepsy (MTLE) remains unknown. Here we used immunohistochemistry, laser scanning confocal microscopy (LSCM), western immunoblotting and RT-PCR to investigate the expression pattern of the alpha-pore forming subunit of BK channels in the hippocampus and cortex of chronically epileptic rats obtained by the pilocarpine model of MTLE. All epileptic rats experiencing recurrent spontaneous seizures exhibited a significant down-regulation of BK channel immunostaining in the mossy fibers at the hilus and stratum lucidum of the CA3 area. Quantitative analysis of immunofluorescence signals by LSCM revealed a significant 47% reduction in BK channel in epileptic rats when compared to age-matched non-epileptic control rats. These data correlate with a similar reduction in BK channel protein levels and transcripts in the cortex and hippocampus. Our data indicate a seizure-related down-regulation of BK channels in chronically epileptic rats. Further functional assays are necessary to determine whether altered BK channel expression is an acquired channelopathy or a compensatory mechanism affecting the network excitability in MTLE. Moreover, seizure-mediated BK down-regulation may disturb neuronal excitability and presynaptic control at glutamatergic terminals triggering exaggerated glutamate release and seizures

Amyloid β peptides modify the expression of antioxidant repair enzymes and a potassium channel in the septohippocampal system

Alzheimer\u27s disease (AD) is a progressive, neurodegenerative brain disorder characterized by extracellular accumulations of amyloid β (Aβ) peptides, intracellular accumulation of abnormal proteins, and early loss of basal forebrain neurons. Recent studies have indicated that the conformation of Aβ is crucial for neuronal toxicity, with intermediate misfolded forms such as oligomers being more toxic than the final fibrillar forms. Our previous work shows that Aβ blocks the potassium (K(+)) currents IM and IA in septal neurons, increasing firing rates, diminishing rhythmicity and firing coherence. Evidence also suggests that oxidative stress (OS) plays a role in AD pathogenesis. Thus we wished to determine the effect of oligomeric and fibrillar forms of Aβ₁₋₄₂ on septohippocampal damage, oxidative damage, and dysfunction in AD. Oligomeric and fibrillar forms of Aβ₁₋₄₂ were injected into the CA1 region of the hippocampus in live rats. The rats were sacrificed 24 hours and 1 month after Aβ or sham injection to additionally evaluate the temporal effects. The expression levels of the K(+) voltage-gated channel, KQT-like subfamily, member 2 (KCNQ₂) and the OS-related genes superoxide dismutase 1, 8-oxoguanine DNA glycosylase, and monamine oxidase A, were analyzed in the hippocampus, medial, and lateral septum. Our results show that both forms of Aβ exhibit time-dependent differential modulation of OS and K(+) channel genes in the analyzed regions. Importantly, we demonstrate that Aβ injected into the hippocampus triggered changes in gene expression in anatomical regions distant from the injection site. Thus the Aβ effect was transmitted to anatomically separate sites, because of the functional coupling of the brain structures

A Non-parametric Approach to Measuring the \kpi{} Amplitudes in \dpkkpi{} Decay

Using a large sample of \dpkkpi{} decays collected by the FOCUS photoproduction experiment at Fermilab, we present the first non-parametric analysis of the \kpi{} amplitudes in \dpkkpi{} decay. The technique is similar to the technique used for our non-parametric measurements of the \krzmndk{} form factors. Although these results are in rough agreement with those of E687, we observe a wider S-wave contribution for the \ksw{} contribution than the standard, PDG \cite{pdg} Breit-Wigner parameterization. We have some weaker evidence for the existence of a new, D-wave component at low values of the $K^- \pi^+$ mass.Comment: 13 pages 3 figure

A Study of D0 --> K0(S) K0(S) X Decay Channels

Using data from the FOCUS experiment (FNAL-E831), we report on the decay of $D^0$ mesons into final states containing more than one $K^0_S$. We present evidence for two Cabibbo favored decay modes, $D^0\to K^0_SK^0_S K^- \pi^+$ and $D^0\to K^0_SK^0_S K^+ \pi^-$, and measure their combined branching fraction relative to $D^0\to \bar{K} ^0\pi^+\pi^-$ to be $\frac{\Gamma(D^0\to K^0_SK^0_SK^{\pm}\pi^{\mp})}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)}$ = 0.0106 $\pm$ 0.0019 $\pm$ 0.0010. Further, we report new measurements of $\frac{\Gamma(D^0\to K^0_SK^0_SK^0_S)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)}$ = 0.0179 $\pm$ 0.0027 $\pm$ 0.0026, $\frac{\Gamma(D^0\to K^0\bar{K} ^0)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)}$ = 0.0144 $\pm$ 0.0032 $\pm$ 0.0016, and $\frac{\Gamma(D^0\to K^0_SK^0_S\pi^+\pi^-)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)}$ = 0.0208 $\pm$ 0.0035 $\pm$ 0.0021 where the first error is statistical and the second is systematic.Comment: 11 pages, 3 figures, typos correcte

Study of Cabibbo Suppressed Decays of the Ds Charmed-Strange Meson involving a KS

We study the decay of Ds meson into final states involving a Ks and report the discovery of Cabibbo suppressed decay modes Ds -> Kspi-pi+pi+ (179 +/- 36 events) and Ds -> Kspi+ (113 +/-26 events). The branching ratios for the new modes are Gamma(Ds -> Kspi-pi+pi+)/Gamma(Ds -> KsK-pi+pi+) = 0.18 +/- 0.04 +/- 0.05 and Gamma(Ds -> Kspi+)/Gamma(Ds -> KsK+) = 0.104 +/- 0.024 +/- 0.013.Comment: 11 pages, 6 figure

The K−π+K^-\pi^+ S-wave from the D+→K−π+π+D^+ \to K^-\pi^+\pi^+ decay

Using data from FOCUS (E831) experiment at Fermilab, we present a model independent partial-wave analysis of the $K^-\pi^+$ S-wave amplitude from the decay $D^+ \to K^-\pi^+\pi^+$. The S-wave is a generic complex function to be determined directly from the data fit. The P- and D-waves are parameterized by a sum of Breit-Wigner amplitudes. The measurement of the S-wave amplitude covers the whole elastic range of the $K^-\pi^+$ system.Comment: 13 pages, 9 figures, submitted to Physics Letters