The Quasi-normal Modes of Charged Scalar Fields in Kerr-Newman black hole and Its Geometric Interpretation

It is well-known that there is a geometric correspondence between high-frequency quasi-normal modes (QNMs) and null geodesics (spherical photon orbits). In this paper, we generalize such correspondence to charged scalar field in Kerr-Newman space-time. In our case, the particle and black hole are all charged, so one should consider non-geodesic orbits. Using the WKB approximation, we find that the real part of quasi-normal frequency corresponds to the orbits frequency, the imaginary part of the frequency corresponds to the Lyapunov exponent of these orbits and the eigenvalue of angular equation corresponds to carter constant. From the properties of the imaginary part of quasi-normal frequency of charged massless scalar field, we can still find that the QNMs of charged massless scalar field possess the zero damping modes in extreme Kerr-Newman spacetime under certain condition which has been fixed in this paper.Comment: 30 pages, many figures, to appear in JHE

Modelling the term structure of Japanese bond yields with the Nelson-Siegel model

The Nelson-Siegel (1987) (NS) model has been credited for its high efficacy in the in-sample fitting and out-of-sample forecasting of the term structures of interest rates. The term structure of interest rates, popularly known as the yield curve, is a static function that relates the time-to-maturity to the yield-to maturity for a sample of bonds at a given point in time. The conventional way of measuring the term structure is by means of the spot rate curve, or yield curve, on zero-coupon bonds. Yet in reality, the entire term structure is not directly observable, which gives rise to the need to estimate it using several approximation techniques. Over the last three decades, various methods to estimate term structures from bond prices have been proposed. In recent years most of the existing studies (as well as major central banks around the globe) have been employing the class of NS models to estimate and construct zero-coupon yield curves. This paper aims to study the term structure of the Japanese bond yields by employing the NS model vs other non-NS models using five different sets of zero-coupon bond yield rates data obtained from the Bank of Japan covering the period spanning from January 2000 to November 2007. This period has been chosen because it clearly exhibits the liquidity trap problem, which forces all bond yields to remain close to zero for an extended period. We propose 18 different NS models, each with different decay components and time series appendages, against 14 other non-NS models ranging from the simple random-walk model to complicated specifications like the VAR and VECM models. A h-period(s)-ahead out-of-sample expanding window forecast is conducted for each of these 32 different models, using daily, weekly and monthly bond yields of 15 different maturities. This study has demonstrated that due to the presence of liquidity trap in Japan, out-of-sample expanding window forecasts in general perform inferiorly vis-à-vis other non-NS models, and this is coupled with the other problem of obtaining negative yield forecasts for bonds with shorter maturities. Moreover, the results show that the NS class of models can be useful in forecasting shorter horizons like weeks and days, works better with a decay rate other than the conventional way of treating it as the value that maximizes the loading on the medium-term factor at exactly 30 months, and can work well with time series models such as GARCH and EGARCH in terms of volatility forecasting. It is also found that, when the NS models are used for yield forecasts, the NS-VAR model should be considered since it is up to par against the competitor models, even with liquidity trap at work

Forecasting term structure of the Japanese bond yields in the presence of a liquidity trap

The Nelson–Siegel (NS) model is widely used in practice to fit the term structure of interest rates largely due to its high efficacy in the in-sample fit and out-of-sample forecasting of bond yields. In this paper, we compare forecasting performances of estimated yields from the Nelson–Siegel-based models and some simpler time series models, using the daily, weekly, and monthly data during a prolong period of liquidity trap in Japan. We find that the out-of-sample expanding window forecasts by NS-based models in general perform less satisfactory than the competitor models. However, the NS-based models can be useful in forecasting yields over longer horizons and can work well with GARCH-type structures in modeling the conditional volatility

Signal regulatory protein alpha initiates cachexia through muscle to adipose tissue crosstalk

BACKGROUND: Muscle wasting from chronic kidney disease (CKD) or from defective insulin signalling results in morbidity and, ultimately, mortality. We have identified an endogenous mediator of insulin resistance, signal regulatory protein alpha (SIRPα), which leads to cachexia in mice and is associated with cachexia in patients with CKD. METHODS: We assessed insulin signalling and mechanisms causing muscle atrophy plus white adipose tissue (WAT) metabolism in mouse models of CKD or acute diabetes (streptozotocin treatment). We then examined these factors in mice with global knockout (KO) of SIRPα and sought mediators of metabolic responses in muscle and adipose tissues of mice with either muscle-specific or adipose tissue-specific KO of SIRPα. Metabolic responses were confirmed in primary cultures of adipose cells. RESULTS: In mice with CKD, SIRPα expression was increased in WAT (three-fold, P \u3c 0.05), and this was associated with precursors of cachexia: \u27pathologic browning\u27, thermogenesis, and a two-fold activation of protein kinase A (P \u3c 0.05 vs. control mice) plus loss of adipose tissue mass. In contrast, mice with SIRPα global KO and CKD or acute diabetes experienced improved insulin signalling and activation of pAkt plus \u27physiologic browning\u27 of WAT. These mice avoided losses of muscle and adipose tissues and experienced a 31% improvement in survival (P \u3c 0.05) than did wild-type mice with CKD. In muscle-specific SIRPα KO mice with CKD, we uncovered that serum SIRPα levels (P \u3c 0.05) were suppressed and were associated with improved insulin signalling both in skeletal muscles and in WAT. These changes were accompanied by physiologic WAT browning. However, in adipose-specific SIRPα KO mice with CKD, levels of serum SIRPα were increased over two-fold (P \u3c 0.05), while muscle losses were minimally inhibited. Clinical implications of SIRPα signalling are suggested by our findings that include increased SIRPα expression in muscle and adipose tissues (P \u3c 0.05 vs. healthy controls) plus higher SIRPα levels in the serum of patients with CKD (2.4-fold, P=0.000017 vs. healthy controls). CONCLUSIONS: Our results show that SIRPα plays an important role as an anti-insulin mediator regulating pathways to cachexia. In muscle-specific SIRPα KO, changes in SIRPα serum levels seem to improve insulin signalling in muscle and WAT, suggesting crosstalk between muscle and adipose tissue. Therefore, targeting SIRPα may prevent cachexia in patients with CKD or acute diabetes

Multifunctional Lateral Transition-Metal Disulfides Heterojunctions

The intrinsic spin-dependent transport properties of two types of lateral VS2|MoS2 heterojunctions are systematically investigated using first-principles calculations, and their various nanodevices with novel properties are designed. The lateral VS2|MoS2 heterojunction diodes show a perfect rectifying effect and are promising for the applications of Schottky diodes. A large spin-polarization ratio is observed for the A-type device and pure spin-mediated current is then realized. The gate voltage significantly tunes the current and rectification ratio of their field-effect transistors (FETs). In addition, they all have sensitive photoresponse to blue light, and could be used as photodetector and photovoltaic device. Moreover, they generate the effective thermally-driven current when a temperature gratitude appears between the two terminals, suggesting them as potential thermoelectric materials. Hence, the lateral VS2|MoS2 heterojunctions show a multifunctional nature and have various potential applications in spintronics, optoelectronics, and spin caloritronics

SIRPα Mediates IGF1 Receptor in Cardiomyopathy Induced by Chronic Kidney Disease

BACKGROUND: Chronic kidney disease (CKD) is characterized by increased myocardial mass despite near-normal blood pressure, suggesting the presence of a separate trigger. A potential driver is SIRPα (signal regulatory protein alpha)-a mediator impairing insulin signaling. The objective of this study is to assess the role of circulating SIRPα in CKD-induced adverse cardiac remodeling. METHODS: SIRPα expression was evaluated in mouse models and patients with CKD. Specifically, mutant, muscle-specific, or cardiac muscle-specific SIRPα KO (knockout) mice were examined after subtotal nephrectomy. Cardiac function was assessed by echocardiography. Metabolic responses were confirmed in cultured muscle cells or cardiomyocytes. RESULTS: We demonstrate that SIRPα regulates myocardial insulin/IGF1R (insulin growth factor-1 receptor) signaling in CKD. First, in the serum of both mice and patients, SIRPα was robustly secreted in response to CKD. Second, cardiac muscle upregulation of SIRPα was associated with impaired insulin/IGF1R signaling, myocardial dysfunction, and fibrosis. However, both global and cardiac muscle-specific SIRPα KO mice displayed improved cardiac function when compared with control mice with CKD. Third, both muscle-specific or cardiac muscle-specific SIRPα KO mice did not significantly activate fetal genes and maintained insulin/IGF1R signaling with suppressed fibrosis despite the presence of CKD. Importantly, SIRPα directly interacted with IGF1R. Next, rSIRPα (recombinant SIRPα) protein was introduced into muscle-specific SIRPα KO mice reestablishing the insulin/IGF1R signaling activity. Additionally, overexpression of SIRPα in myoblasts and cardiomyocytes impaired pAKT (phosphorylation of AKT) and insulin/IGF1R signaling. Furthermore, myotubes and cardiomyocytes, but not adipocytes treated with high glucose or cardiomyocytes treated with uremic toxins, stimulated secretion of SIRPα in culture media, suggesting these cells are the origin of circulating SIRPα in CKD. Both intracellular and extracellular SIRPα exert biologically synergistic effects impairing intracellular myocardial insulin/IGF1R signaling. CONCLUSIONS: Myokine SIRPα expression impairs insulin/IGF1R functions in cardiac muscle, affecting cardiometabolic signaling pathways. Circulating SIRPα constitutes an important readout of insulin resistance in CKD-induced cardiomyopathy