A power-law coupled three-form dark energy model

We consider a field theory model of coupled dark energy which treats dark energy as a three-form field and dark matter as a spinor field. By assuming the effective mass of dark matter as a power-law function of the three-form field and neglecting the potential term of dark energy, we obtain three solutions of the autonomous system of evolution equations, including a de Sitter attractor, a tracking solution and an approximate solution. To understand the strength of the coupling, we confront the model with the latest Type Ia Supernova (SN Ia), Baryon Acoustic Oscillations (BAO) and Cosmic Microwave Backround (CMB) radiation observations, with the conclusion that the combination of these three databases marginalized over the present dark matter density parameter $\Omega_{m0}$ and the present three-form field $\kappa X_{0}$ gives stringent constraints on the coupling constant, $-0.017< \lambda <0.047$ ($2\sigma$ confidence level), by which we give out the model applicable parameter range.Comment: 16 pages, 5 figures, refernces added, Eur. Phys. J. C (2018

Transformation of \u3cem\u3eTetrahymena thermophila\u3c/em\u3e with Hypermethylated rRNA Genes

The extrachromosomal rRNA genes (rDNA) of Tetrahymena thermophila contain 0.4% N6-methyladenine. C3 strain rDNA was isolated, hypermethylated in vitro, and microinjected into B strain host cells. Clonal cell lines were established, and transformants were selected on the basis of resistance to paromomycin, conferred by the injected rDNA. The effects of methylation by three enzymes which methylate the sequence 5\u27-NAT-3\u27, the dam, EcoRI, and ClaI methylases, were tested. Hypermethylation of the injected rDNA had no effect on transformation efficiency relative to mock-methylated controls. The injected C3 strain rDNA efficiently replaced host rDNA as the major constituent of the population of rDNA molecules. Hypermethylation of the injected DNA was not maintained through 20 to 25 cell generations

A Complementary Third Law for Black Hole Thermodynamics

There are some examples in the literature, in which despite the fact that the underlying theory or model does not impose a lower bound on the size of black holes, the final temperature under Hawking evaporation is nevertheless finite and nonzero. We show that under some loose conditions, the black hole is necessarily an effective remnant, in the sense that its evaporation time is infinite. That is, the final state that there is nonzero finite temperature despite having no black hole remaining cannot be realized. We discuss the limitations, subtleties, and the implications of this result, which is reminiscent of the third law of black hole thermodynamics, but with the roles of temperature and size interchanged. We therefore refer to our result as the "complementary third law" for black hole thermodynamics.Comment: 10 pages, 5 figures; improved and published versio

Studies on X(4260) and X(4660) particles

Studies on the X(4260) and X(4660) resonant states in an effective lagrangian approach are reviewed. Using a Breit--Wigner propagator to describe their propagation, we find that the X(4260) has a sizable coupling to the $\omega\chi_{c0}$ channel, while other couplings are found to be negligible. Besides, it couples much stronger to $\sigma$ than to $f_0(980)$: $|g_{X\Psi \sigma}^2/g^2_{X\Psi f_0(980)}|\sim O(10) \ .$ As an approximate result for X(4660), we obtain that the ratio of $\frac{Br(X\rightarrow\Lambda_c^+\Lambda_c^-)}{Br(X\rightarrow\Psi(2s)\pi^+\pi^-)}\simeq 20$. Finally, taking X(3872) as an example, we also point out a possible way to extend the previous method to a more general one in the effective lagrangian approach.Comment: Talk given by H. Q. Zheng at "Xth Quark Confinement and the Hadron Spectrum", October 8-12, 2012, TUM Campus Garching, Munich, Germany. 6 pages, 3 figures, 3 table

Aldosterone-induced changes in endothelial function

Patients with primary aldosteronism (PA) are characterized by an excess of cardiovascular morbidities independent of the degree of associated arterial hypertension. These comorbidities share the same etiology as the sequelae of atherosclerosis of which endothelial dysfunction is considered to be the initiating step. Endothelial cells feature a variety of pathways to relax vas-cular smooth muscle and maintain a healthy vascular homeostasis, one of the pathways being the epoxyeicosatrienoic acid (EET) pathway as a component of the endothelium-derived hy-perpolarizing factor (EDHF) family. At present, little is known about whether primary aldosteron-ism affects EET release from endothelial cells. Knowledge about the EET pathway functional integrity could translate to therapeutic applications targeting EET breakdown to ultimately target the cardiovascular comorbidities observed in PA. Endothelial mineralocorticoid receptors are exposed not only to aldosterone but also to circulat-ing glucocorticoids at much higher concentrations. 11-β-HSD (hydroxysteroid dehydrogenase) type 2 protects mineralocorticoid receptors from glucocorticoids in a cell-type specific manner. Significant knowledge gaps still exist with regard to the role of this glucocorticoid inactivation system in endothelial cells and its role in mineralocorticoid excess. The aims of this project were (A) to investigate a potential impairment of endothelium-derived vasoactive EETs in a context of aldosterone-induced endothelial dysfunction and (B) to deter-mine the existence and the degree of endothelial gluco- and mineralocorticoid receptor transac-tivation. It could be shown that endothelial cells exposed to aldosterone excess retain their original ex-pression levels of enzymes critical for the synthesis and degradation of EETs. On the other hand, aldosterone increased expression levels of a mesenchymal marker gene and impaired calcium response to stimulation by acetylcholine, thereby underpinning the biological activity of the steroid concentrations which were used. Despite these broad changes in endothelial physi-ology, stimulated secretion of EETs into the endothelial supernatant was unchanged in condi-tions of aldosterone excess, arguing for an undisturbed endothelial EET pathway in primary aldosteronism. Because of the seemingly unimpaired EET synthesis, inhibition of EET break-down may therefore be a reasonable therapeutic option in treating vascular disease in primary aldosteronism. With respect to aim (B), qPCR revealed negligible expression levels of both 11-β-HSD type 1 or 11-β-HSD type 2. These data could be corroborated functionally by measurements of cortisone and cortisol in the supernatants. Aldosterone at various concentrations did not modulate the expression or activity of both 11-β-HSD enzymes. Traditional markers of transcriptional activity of mineralocorticoid and glucocorticoid receptors turned out to be not useful for endothelial cells, since they could not be shown to be affected by stimulation with cortisol and aldosterone. A semiquantitative, immunofluorescence-based nuclear localization assay of steroid receptors as global readout of activity was established. This assay revealed that aldosterone antagonized nuclear translocation of glucocorticoid receptors in a mineralocorticoid receptor-dependent manner. This novel finding suggests that under certain circumstances mineralocorticoids might antagonize glucocorticoids and highlights the complex interaction between both corticosteroids. Future studies will apply the developed assay to tissues derived from patients harboring single and combined excessive secretion of gluco- and mineralocorticoids to further investigate steroid interactions in endothelial cells following in vivo exposure