Tuning the stochastic background of gravitational waves using the WMAP data

The cosmological bound of the stochastic background of gravitational waves is analyzed with the aid of the WMAP data, differently from lots of works in literature, where the old COBE data were used. From our analysis, it will result that the WMAP bounds on the energy spectrum and on the characteristic amplitude of the stochastic background of gravitational waves are greater than the COBE ones, but they are also far below frequencies of the earth-based antennas band. At the end of this letter a lower bound for the integration time of a potential detection with advanced LIGO is released and compared with the previous one arising from the old COBE data. Even if the new lower bound is minor than the previous one, it results very long, thus for a possible detection we hope in the LISA interferometer and in a further growth in the sensitivity of advanced projects.Comment: 9 pages, 2 figures, published in Modern Physics Letters A. arXiv admin note: substantial text overlap with arXiv:0901.119

Alternative livelihoods in a coastal village

Women, Gender, Economic situation, Philippines,

Removing black-hole singularities with nonlinear electrodynamics

We propose a way to remove black hole singularities by using a particular nonlinear electrodynamics Lagrangian that has been recently used in various astrophysics and cosmological frameworks. In particular, we adapt the cosmological analysis discussed in a previous work to the black hole physics. Such analysis will be improved by applying the Oppenheimer-Volkoff equation to the black hole case. At the end, fixed the radius of the star, the final density depends only on the introduced quintessential density term $\rho_{\gamma}$ and on the mass.Comment: In this last updated version we correct two typos which were present in Eqs. (21) and (22) in the version of this letter which has been published in Mod. Phys. Lett. A 25, 2423-2429 (2010). In the present version, both of Eqs. (21) and (22) are dimensionally and analytically correc

A precise response function for the magnetic component of Gravitational Waves in Scalar-Tensor Gravity

The important issue of the magnetic component of gravitational waves (GWs) has been considered in various papers in the literature. From such analyses, it resulted that such a magnetic component becomes particularly important in the high frequency portion of the frequency range of ground based interferometers for GWs which arises from standard General Theory of Relativity (GTR). Recently, such a magnetic component has been extended to GWs arising from Scalar-Tensor Gravity (STG) too. After a review of some important issues on GWs in STG, in this paper we re-analyse the magnetic component in the framework of STG from a different point of view, by correcting an error in a previous paper and by releasing a more precise response function. In this way, we also show that if one neglects the magnetic contribution considering only the low-frequency approximation of the electric contribution, an important part of the signal could be, in principle, lost. The determination of a more precise response function for the magnetic contribution is important also in the framework of the possibility to distinguish other gravitational theories from GTR. At the end of the paper an expansion of the main results is also shown in order to recall the presence of the magnetic component in GRT too.Comment: Accepted for publication in Physical Review D, to be published during 2011. 36 pages, in this second version typos have been corrected and references have been update

Characterization of a disease-associated mutation affecting a putative splicing regulatory element in intron 6b of the cystic fibrosis transmembrane conductance regulator (CFTR) gene

Cystic fibrosis (CF) is a common recessive disorder caused by >1600 mutations in the CF transmembrane conductance regulator (CFTR) gene. About 13% of CFTR mutations are classified as “splicing mutations,” but for almost 40% of these, their role in affecting the pre-mRNA splicing of the gene is not yet defined. In this work, we describe a new splicing mutation detected in three unrelated Italian CF patients. By DNA analyses and mRNA studies, we identified the c.1002–1110_1113delTAAG mutation localized in intron 6b of the CFTR gene. At the mRNA level, this mutation creates an aberrant inclusion of a sequence of 101 nucleotides between exons 6b and 7. This sequence corresponds to a portion of intron 6b and resembles a cryptic exon because it is characterized by an upstream ag and a downstream gt sequence, which are most probably recognized as 5′- and 3′-splice sites by the spliceosome. Through functional analysis of this splicing defect, we show that this mutation abolishes the interaction of the splicing regulatory protein heterogeneous nuclear ribonucleoprotein A2/B1 with an intronic splicing regulatory element and creates a new recognition motif for the SRp75 splicing factor, causing activation of the cryptic exon. Our results show that the c.1002–1110_1113delTAAG mutation creates a new intronic splicing regulatory element in intron 6b of the CFTR gene exclusively recognized by SRp75

Glycerophosphoinositol 4-phosphate, a putative endogenous inhibitor of adenylylcyclase.

In a continuous line of rat thyroid cells transformed by the k-ras oncogene (KiKi), the expression of ras-p21 correlates with an increased activity of a phosphoinositide-specific phospholipase A2, which leads to elevated levels of glycerophosphoinositols. In this study we have characterized the biological activities of these compounds. Growth and differentiation in thyroid cells are mainly regulated by the activation of adenylylcyclase. Therefore, we have studied the effects of glycerophosphoinositols on the activity of this enzyme using a normal thyroid cell line (FRTL5). Micromolar concentrations of glycerophosphoinositol 4-phosphate (GroPIns-4-P) caused a approximately 50% inhibition of the adenylylcyclase activity in FRTL5 membranes stimulated by the GTP-binding protein activator fluoroaluminate. Similar concentrations of GroPIns-4-P were detected in KiKi cells but not in the normal FRTL5 line. Micromolar GroPIns-4-P was found to be taken up by intact FRTL5 cells and to induce nearly 50% inhibition of the thyrotropin- and cholera toxin-induced increase in cAMP levels. Similar results were also observed in other cell lines (smooth muscle, pituitary cells, and pneumocytes). GroPIns-4-P inhibited cAMP-dependent cellular functions such as iodide uptake and thymidine incorporation in FRTL5 cells when stimulated by thyrotropin and cholera toxin but not when induced by forskolin. These results are consistent with GroPIns-4-P exerting an inhibitory effect on the GTP-binding protein that stimulates adenylycyclase. We propose that GroPIns-4-P might mediate a mechanism of cross-talk between adenylylcyclase and phospholipase A2 in thyroid as well as in other cell systems

Three new Alpha1-Antitrypsin deficiency variants help to define a C-Terminal region regulating conformational change and polymerization

Alpha1-antitrypsin (AAT) deficiency is a hereditary disorder associated with reduced AAT plasma levels, predisposing adults to pulmonary emphysema. The most common genetic AAT variants found in patients are the mildly deficient S and the severely deficient Z alleles, but several other pathogenic rare alleles have been reported. While the plasma AAT deficiency is a common trait of the disease, only a few AAT variants, including the prototypic Z AAT and some rare variants, form cytotoxic polymers in the endoplasmic reticulum of hepatocytes and predispose to liver disease. Here we report the identification of three new rare AAT variants associated to reduced plasma levels and characterize their molecular behaviour in cellular models. The variants, called Mpisa (Lys259Ile), Etaurisano (Lys368Glu) and Yorzinuovi (Pro391His), showed reduced secretion compared to control M AAT, and accumulated to different extents in the cells as ordered polymeric structures resembling those formed by the Z variant. Structural analysis of the mutations showed that they may facilitate polymerization both by loosening ‘latch’ interactions constraining the AAT reactive loop and through effects on core packing. In conclusion, the new AAT deficiency variants, besides increasing the risk of lung disease, may predispose to liver disease, particularly if associated with the common Z variant. The new mutations cluster structurally, thus defining a region of the AAT molecule critical for regulating its conformational state

Some exact solutions of F(R) gravity with charged (a)dS black hole interpretation

In this paper we obtain topological static solutions of some kind of pure $F(R)$ gravity. The present solutions are two kind: first type is uncharged solution which corresponds with the topological (a)dS Schwarzschild solution and second type has electric charge and is equivalent to the Einstein-$\Lambda$-conformally invariant Maxwell solution. In other word, starting from pure gravity leads to (charged) Einstein-$\Lambda$ solutions which we interpreted them as (charged) (a)dS black hole solutions of pure $F(R)$ gravity. Calculating the Ricci and Kreschmann scalars show that there is a curvature singularity at $r=0$. We should note that the Kreschmann scalar of charged solutions goes to infinity as $r \rightarrow 0$, but with a rate slower than that of uncharged solutions.Comment: 21 pages, 4 figures, generalization to higher dimensions, references adde

Association of the changes in cytosolic Ca2+ and iodide efflux induced by thyrotropin and by the stimulation of alpha 1-adrenergic receptors in cultured rat thyroid cells.

Abstract Thyrotropin causes a time- and concentration-dependent increase in cytosolic Ca2+ in FRTL-5 rat thyroid cells as measured by Quin2 fluorescence; the half-maximal response occurs in response to 1 X 10(-7) M thyrotropin. The effect of added thyrotropin is the same whether cells have been previously and chronically exposed to thyrotropin or whether they have been thyrotropin "starved" for several days. The thyrotropin effect on cytosolic Ca2+ has no relationship to intracellular cAMP levels with respect to dose and time course. Norepinephrine (1 X 10(-7) M) also causes increases in cytosolic Ca2+ in FRTL-5 thyroid cells. With the use of a variety of adrenergic inhibitors, norepinephrine was found to exert its effect via an alpha 1-adrenergic receptor. The exposure of FRTL-5 cells to physiological thyrotropin concentrations enhances the effect on cytosolic Ca2+ level induced by norepinephrine in vitro; the shape of the dose-response curve indicates a cooperative effect of the thyrotropin and norepinephrine. The increase in cytosolic Ca2+ seems to be derived from an intracellular pool rather than from the extracellular space. It is not prevented by nifedipine, a blocker of Ca2+ channels; it is present in cells exposed to ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid; and it is not associated with increased Ca2+ uptake into the cell. the thyrotropin- and norepinephrine-induced increase in cytosolic Ca2+ parallels the efflux of iodide and the organification of thyroglobulin in a dose-dependent manner