Phantom Cosmology with Non-minimally Coupled Real Scalar Field

We find that the expansion of the universe is accelerating by analyzing the recent observation data of type \textsc{I}a supernova(SN-Ia) .It indicates that the equation of state of the dark energy might be smaller than -1,which leads to the introduction of phantom models featured by its negative kinetic energy to account for the regime of equation of state parameter $w<-1$.In this paper the possibility of using a non-minimally coupled real scalar field as phantom to realize the equation of state parameter $w<-1$ is discussed.The main equations which govern the evolution of the universe are obtained.Then we rewrite them with the observable quantities.Comment: 12 pages, 2 figures. Accepted for publication in Gen.Rel.Gra

Chronic Stress Induces Maladaptive Behaviors by Activating Corticotropin-Releasing Hormone Signaling in the Mouse Oval Bed Nucleus of the Stria Terminalis

The bed nucleus of the stria terminalis (BNST) is a forebrain region highly responsive to stress that expresses corticotropin-releasing hormone (CRH) and is implicated in mood disorders, such as anxiety. However, the exact mechanism by which chronic stress induces CRH-mediated dysfunction in BNST and maladaptive behaviors remains unclear. Here, we first confirmed that selective acute optogenetic activation of the oval nucleus BNST (ovBNST) increases maladaptive avoidance behaviors in male mice. Next, we found that a 6 week chronic variable mild stress (CVMS) paradigm resulted in maladaptive behaviors and increased cellular excitability of ovBNST CRH neurons by potentiating mEPSC amplitude, altering the resting membrane potential, and diminishing M-currents (a voltage-gated K+ current that stabilizes membrane potential) in ex vivo slices. CVMS also increased c-fos+ cells in ovBNST following handling. We next investigated potential molecular mechanism underlying the electrophysiological effects and observed that CVMS increased CRH+ and pituitary adenylate cyclase-activating polypeptide+ (PACAP; a CRH upstream regulator) cells but decreased striatal-enriched protein tyrosine phosphatase+ (a STEP CRH inhibitor) cells in ovBNST. Interestingly, the electrophysiological effects of CVMS were reversed by CRHR1-selective antagonist R121919 application. CVMS also activated protein kinase A (PKA) in BNST, and chronic infusion of the PKA-selective antagonist H89 into ovBNST reversed the effects of CVMS. Coadministration of the PKA agonist forskolin prevented the beneficial effects of R121919. Finally, CVMS induced an increase in surface expression of phosphorylated GluR1 (S845) in BNST. Collectively, these findings highlight a novel and indispensable stress-induced role for PKA-dependent CRHR1 signaling in activating BNST CRH neurons and mediating maladaptive behaviors

Quantum coherence in a degenerate two-level atomic ensemble: for a transition Fe=0↔Fg=1F_e=0\leftrightarrow F_g=1

For a transition $F_e=0\leftrightarrow F_g=1$ driven by a linearly polarized light and probed by a circularly light, quantum coherence effects are investigated. Due to the coherence between the drive Rabi frequency and Zeeman splitting, electromagnetically induced transparency, electromagnetically induced absorption, and the transition from positive to negative dispersion are obtained, as well as the populations coherently oscillating in a wide spectral region. At the zero pump-probe detuning, the subluminal and superluminal light propagation is predicted. Finally, coherent population trapping states are not highly sensitive to the refraction and absorption in such ensemble.Comment: 9 pages, 6 figure

Phantom Field with O(N) Symmetry in Exponential Potential

In this paper, we study the phase space of phantom model with O(\emph{N}) symmetry in exponential potential. Different from the model without O(\emph{N}) symmetry, the introduction of the symmetry leads to a lower bound $w>-3$ on the equation of state for the existence of stable phantom dominated attractor phase. The reconstruction relation between the potential of O(\textit{N}) phantom system and red shift has been derived.Comment: 5 pages, 3 figures, replaced with the version to appear on Phys. Rev.

Linear and non-linear perturbations in dark energy models

I review the linear and second-order perturbation theory in dark energy models with explicit interaction to matter in view of applications to N-body simulations and non-linear phenomena. Several new or generalized results are obtained: the general equations for the linear perturbation growth; an analytical expression for the bias induced by a species-dependent interaction; the Yukawa correction to the gravitational potential due to dark energy interaction; the second-order perturbation equations in coupled dark energy and their Newtonian limit. I also show that a density-dependent effective dark energy mass arises if the dark energy coupling is varying.Comment: 12 pages, submitted to Phys. Rev; v2: added a ref. and corrected a typ

Neutrino clustering in growing neutrino quintessence

A growing neutrino mass can stop the dynamical evolution of a dark energy scalar field, thus explaining the 'why now' problem. We show that such models lead to a substantial neutrino clustering on the scales of superclusters. Nonlinear neutrino lumps form at redshift z \sim 1 and could partially drag the clustering of dark matter. If observed, large scale non-linear structures could be an indication for a new attractive 'cosmon force' stronger than gravity.Comment: 6 pages, 5 figure

A somatic-mutational process recurrently duplicates germline susceptibility loci and tissue-specific super-enhancers in breast cancers

Somatic rearrangements contribute to the mutagenized landscape of cancer genomes. Here, we systematically interrogated rearrangements in 560 breast cancers by using a piecewise constant fitting approach. We identified 33 hotspots of large (>100 kb) tandem duplications, a mutational signature associated with homologous-recombination-repair deficiency. Notably, these tandem-duplication hotspots were enriched in breast cancer germline susceptibility loci (odds ratio (OR) = 4.28) and breast-specific 'super-enhancer' regulatory elements (OR = 3.54). These hotspots may b

Trans-ancestry genome-wide association study identifies 12 genetic loci influencing blood pressure and implicates a role for DNA methylation

We carried out a trans-ancestry genome-wide association and replication study of blood pressure phenotypes among up to 320,251 individuals of East Asian, European and South Asian ancestry. We find genetic variants at 12 new loci to be associated with blood pressure (P = 3.9 &times; 10-11 to 5.0 &times; 10-21). The sentinel blood pressure SNPs are enriched for association with DNA methylation at multiple nearby CpG sites, suggesting that, at some of the loci identified, DNA methylation may lie on the regulatory pathway linking sequence variation to blood pressure. The sentinel SNPs at the 12 new loci point to genes involved in vascular smooth muscle (IGFBP3, KCNK3, PDE3A and PRDM6) and renal (ARHGAP24, OSR1, SLC22A7 and TBX2) function. The new and known genetic variants predict increased left ventricular mass, circulating levels of NT-proBNP, and cardiovascular and all-cause mortality (P = 0.04 to 8.6 &times; 10-6). Our results provide new evidence for the role of DNA methylation in blood pressure regulation

AD51B in Familial Breast Cancer

Common variation on 14q24.1, close to RAD51B, has been associated with breast cancer: rs999737 and rs2588809 with the risk of female breast cancer and rs1314913 with the risk of male breast cancer. The aim of this study was to investigate the role of RAD51B variants in breast cancer predisposition, particularly in the context of familial breast cancer in Finland. We sequenced the coding region of RAD51B in 168 Finnish breast cancer patients from the Helsinki region for identification of possible recurrent founder mutations. In addition, we studied the known rs999737, rs2588809, and rs1314913 SNPs and RAD51B haplotypes in 44,791 breast cancer cases and 43,583 controls from 40 studies participating in the Breast Cancer Association Consortium (BCAC) that were genotyped on a custom chip (iCOGS). We identified one putatively pathogenic missense mutation c.541C&gt;T among the Finnish cancer patients and subsequently genotyped the mutation in additional breast cancer cases (n = 5259) and population controls (n = 3586) from Finland and Belarus. No significant association with breast cancer risk was seen in the meta-analysis of the Finnish datasets or in the large BCAC dataset. The association with previously identified risk variants rs999737, rs2588809, and rs1314913 was replicated among all breast cancer cases and also among familial cases in the BCAC dataset. The most significant association was observed for the haplotype carrying the risk-alleles of all the three SNPs both among all cases (odds ratio (OR): 1.15, 95% confidence interval (CI): 1.11–1.19, P = 8.88 x 10−16) and among familial cases (OR: 1.24, 95% CI: 1.16–1.32, P = 6.19 x 10−11), compared to the haplotype with the respective protective alleles. Our results suggest that loss-of-function mutations in RAD51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk