Quantum dynamical correlations: Effective potential analytic continuation approach

We propose a new quantum dynamics method called the effective potential analytic continuation (EPAC) to calculate the real time quantum correlation functions at finite temperature. The method is based on the effective action formalism which includes the standard effective potential. The basic notions of the EPAC are presented for a one-dimensional double well system in comparison with the centroid molecular dynamics (CMD) and the exact real time quantum correlation function. It is shown that both the EPAC and the CMD well reproduce the exact short time behavior, while at longer time their results deviate from the exact one. The CMD correlation function damps rapidly with time because of ensemble dephasing. The EPAC correlation function, however, can reproduce the long time oscillation inherent in the quantum double well systems. It is also shown that the EPAC correlation function can be improved toward the exact correlation function by means of the higher order derivative expansion of the effective action.Comment: RevTeX4, 20 pages, 6 eps figure

Prospects for improving the sensitivity of KAGRA gravitational wave detector

KAGRA is a new gravitational wave detector which aims to begin joint observation with Advanced LIGO and Advanced Virgo from late 2019. Here, we present KAGRA's possible upgrade plans to improve the sensitivity in the decade ahead. Unlike other state-of-the-art detectors, KAGRA requires different investigations for the upgrade since it is the only detector which employs cryogenic cooling of the test mass mirrors. In this paper, investigations on the upgrade plans which can be realized by changing the input laser power, increasing the mirror mass, and injecting frequency dependent squeezed vacuum are presented. We show how each upgrade affects to the detector frequency bands and also discuss impacts on gravitational-wave science. We then propose an effective progression of upgrades based on technical feasibility and scientific scenarios

Gravitational waves from the remnants of the first stars

Gravitational waves (GWs) provide a revolutionary tool to investigate yet unobserved astrophysical objects. Especially the first stars, which are believed to be more massive than present-day stars, might be indirectly observable via the merger of their compact remnants. We develop a self-consistent, cosmologically representative, semi-analytical model to simulate the formation of the first stars. By extrapolating binary stellar-evolution models at 10 per cent solar metallicity to metal-free stars, we track the individual systems until the coalescence of the compact remnants. We estimate the contribution of primordial stars to the merger rate density and to the detection rate of the Advanced Laser Interferometer Gravitational-Wave Observatory (aLIGO). Owing to their higher masses, the remnants of primordial stars produce strong GW signals, even if their contribution in number is relatively small. We find a probability of greater than or similar to 1 per cent that the current detection GW150914 is of primordial origin. We estimate that aLIGO will detect roughly 1 primordial BH-BH merger per year for the final design sensitivity, although this rate depends sensitively on the primordial initial mass function (IMF). Turning this around, the detection of black hole mergers with a total binary mass of similar to 300 M-circle dot would enable us to constrain the primordial IMF

The role of thyroid hormone nuclear receptors in the heart: evidence from pharmacological approaches

This review evaluates the hypothesis that the cardiac effects of amiodarone can be explained—at least partly—by the induction of a local ‘hypothyroid-like condition’ in the heart. Evidence supporting the hypothesis comprises the observation that amiodarone exerts an inhibitory effect on the binding of T3 to thyroid hormone receptors (TR) alpha-1 and beta-1 in vitro, and on the expression of particular T3-dependent genes in vivo. In the heart, amiodarone decreases heart rate and alpha myosin heavy chain expression (mediated via TR alpha-1), and increases sarcoplasmic reticulum calcium-activated ATPase and beta myosin heavy chain expression (mediated via TR beta-1). Recent data show a significant similarity in expression profiles of 8,435 genes in the heart of hypothyroid and amiodarone-treated animals, although similarities do not always exist in transcripts of ion channel genes. Induction of a hypothyroid cardiac phenotype by amiodarone may be advantageous by decreasing energy demands and increasing energy availability

Absence of Myocardial Thyroid Hormone Inactivating Deiodinase Results in Restrictive Cardiomyopathy in Mice

Cardiac injury induces myocardial expression of the thyroid hormone inactivating type 3 deiodinase (D3), which in turn dampens local thyroid hormone signaling. Here, we show that the D3 gene (Dio3) is a tissue-specific imprinted gene in the heart, and thus, heterozygous D3 knockout (HtzD3KO) mice constitute a model of cardiac D3 inactivation in an otherwise systemically euthyroid animal. HtzD3KO newborns have normal hearts but later develop restrictive cardiomyopathy due to cardiac-specific increase in thyroid hormone signaling, including myocardial fibrosis, impaired myocardial contractility, and diastolic dysfunction. In wild-type littermates, treatment with isoproterenol-induced myocardial D3 activity and an increase in the left ventricular volumes, typical of cardiac remodeling and dilatation. Remarkably, isoproterenol-treated HtzD3KO mice experienced a further decrease in left ventricular volumes with worsening of the diastolic dysfunction and the restrictive cardiomyopathy, resulting in congestive heart failure and increased mortality. These findings reveal crucial roles for Dio3 in heart function and remodeling, which may have pathophysiologic implications for human restrictive cardiomyopathy

Cardiomyocyte-specific inactivation of thyroid hormone in pathologic ventricular hypertrophy: an adaptative response or part of the problem?

Recent studies in various rodent models of pathologic ventricular hypertrophy report the re-expression of deiodinase type 3 (D3) in cardiomyocytes. D3 inactivates thyroid hormone (T3) and is mainly expressed in tissues during development. The stimulation of D3 activity in ventricular hypertrophy and subsequent heart failure is associated with severe impairment of cardiac T3 signaling. Hypoxia-induced signaling appears to drive D3 expression in the hypertrophic cardiomyocyte, but other signaling cascades implicated in hypertrophy are also capable of stimulating transcription of the DIO3 gene. Many cardiac genes are transcriptionally regulated by T3 and impairment of T3 signaling will not only reduce energy turnover, but also lead to changes in gene expression that contribute to contractile dysfunction in pathologic remodeling. Whether stimulation of D3 activity and the ensuing local T3-deficiency is an adaptive response of the stressed heart or part of the pathologic signaling network leading to heart failure, remains to be established