121 research outputs found

    A theory of the non-neutrality of money with banking frictions and bank recapitalization

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    The unconventional monetary policy actions of the Federal Reserve during the recent Global Financial Crisis often involve implicit subsidies to banks. This paper offers a theory of the non-neutrality of money associated with capital injection into banks via nominal transfers, in an environment where banking frictions are present in the sense that there exists an agency problem between banks and their private-sector creditors. The analysis is conducted within a general equilibrium setting with two-sided financial contracting. We first show that even with perfect nominal flexibility, the recapitalization policy has real effects on the economy. We then introduce banking riskiness shocks and study optimal policy responses to such shocks.Bankruptcy of banks; banking riskiness shocks; two-sided debt contract; unconventional monetary policy; financial crisis

    The Financial and Macroeconomic Implications of Banking Frictions and Banking Riskiness

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    This paper develops a model of banking frictions and banking riskiness, the importance of which is highlighted by the recent Global Financial Crisis (GFC). We propose a model-based approach to decompose the effect of a banking riskiness shock into a pure default effect and a risk effect when risk sharing among the depositors is imperfect. Although the default effect is quantitatively more important, the risk effect is not to be neglected. When the shock generates a bank spread similar in value to the peak during the GFC, the overall effect is a decline in employment by 6:57 percent. The pure default effect leads to a 4:76 percent employment decline by a “within-model” measure, and a 5:05 decline by a “between-model” measure. The remaining is attributed to the risk effect.Banking riskiness shocks; two-sided debt contract; default effects; risk effects; financial crisis.

    Asset Prices, Monetary Policy, and Aggregate Fluctuations: An Empirical Investigation

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    This paper studies empirically the dynamic interactions between asset prices, monetary policy, and aggregate fluctuations during the Volcker-Greenspan period. Using a simple structural vector autoregression framework, we investigate the effects of monetary policy on output, inflation and asset prices, the interactions of asset prices with the aggregate economy, as well as the relationship between stock price and house price. Several robust findings emerge. The systematic response of monetary policy to output and inflation is also found to play an important role in stabilizing the aggregate economy. In addition, the results call for special attention to be paid to house price when studying the dynamic relationships between asset prices and macroeconomic fluctuations.House prices; stock prices; systematic monetary policy; structural vector autoregressions.

    A theory of the non-neutrality of money with banking frictions and bank recapitalization

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    Policy actions by the Federal Reserve during the recent financial crisis often involve recapitalization of banks. This paper offers a theory of the non-neutrality of money for policy actions taking the form of injecting capital into banks via nominal transfers, in an environment where banking frictions are present in the sense that there exists an agency cost problem between banks and their private-sector creditors. The analysis is conducted within a general equilibrium setting with two-sided financial contracting. We first show that even with perfect nominal flexibility, the recapitalization policy can have real effects on the economy. We then study the design of the optimal long-run recapitalization policy as well as the optimal short-run policy responses to banking riskiness shocks.Banking frictions; two-sided debt contract; money neutrality; unconventional monetary policy; reaction function.

    Real Estate, the External Finance Premium and Business Investment: A Quantitative Dynamic General Equilibrium Analysis

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    This paper studies the connection between the capital market and the real estate market. Empirically, we find that positive real house price shocks lower the external finance premium and stimulate nonresidential investment and real GDP. Our theoretical framework is able to mimic the volatility of the external finance premium, the relative price of real estate and capital, and the investment in real estate and capital. It also captures the cyclicality of the external finance premium and of real estate prices. The contribution of real estate price fluctuations to the variability of the external finance premium and the GDP is confirmed to be significant.External Finance Premium, Residential and Corporate Real Estate, Capital Market Imperfections, Equilibrium Default, Real Estate Price Volatility.

    A theory of the non-neutrality of money with banking frictions and bank recapitalization

    Get PDF
    The unconventional monetary policy actions of the Federal Reserve during the recent Global Financial Crisis often involve implicit subsidies to banks. This paper offers a theory of the non-neutrality of money associated with capital injection into banks via nominal transfers, in an environment where banking frictions are present in the sense that there exists an agency problem between banks and their private-sector creditors. The analysis is conducted within a general equilibrium setting with two-sided financial contracting. We first show that even with perfect nominal flexibility, the recapitalization policy has real effects on the economy. We then introduce banking riskiness shocks and study optimal policy responses to such shocks

    A Novel SASH1-IQGAP1-E-Cadherin Signal Cascade Mediates Breast Cancer Metastasis

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    SAM and SH3 domain-containing protein 1 (SASH1) was previously described as a candidate tumor suppressor gene in breast cancer and colon cancer to mediate tumor metastasis and tumor growth. However, the underlying mechanism that SASH1 implements breast cancer metastasis in most solid cancers remains unexplored. In this study, SASH1 was identified to bind to IQ motif-containing GTPase activating protein 1 (IQGAP1). In breast cancer tissues, there was a correlation between the expressions of SASH1 and IQGAP1 (P  0.05). Therefore, it is suggested that SASH1 may form a new signaling cascade with IQGAP1 and E-cadherin to regulate breast cancer metastasis

    Experimental Study on the Deactivating Effect of KNO 3

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    Nanosized Ce/TiO2 is effective in selective catalytic reduction of NO with NH3. The NO conversion of Ce/TiO2 is 93% at 370°C. However, addition of potassium using KNO3, KCl, or K2SO4 as precursors effectively deactivates Ce/TiO2. NO conversion at 370°C is reduced to 45%, 24%, and 16% after addition of KNO3, KCl, and K2SO4, respectively, with a controlled K/Ce molar ration at 0.25. The deactivation may be attributed to the changes in the structural and chemical state of ceria and the degradation of surface acidity. The transformation of amorphous ceria into ceria crystals after potassium addition, together with the decrease of surface defects, is also determined. Oxygen diffusion in the process of ceria reduction is slow, and the redox cycle is slowed down. Moreover, the surface acid sites are markedly destroyed, leading to the reduced capacity of ammonia adsorption. These results may provide useful information for the application and life management of CeO2/TiO2 in potassium-rich environments such as biofuel-fired boilers

    A Novel P53/POMC/Gas/SASH1 Autoregulatory Feedback Loop and Pathologic Hyperpigmentation

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    P53-regulated proteins in transcriptional level are associated with many signal transduction pathways and p53 plays a pivotal role in a number of positive and negative autoregulatory feedback loops. Although POMC/α-MSH productions induced by ultraviolet (UV) are directly mediated by p53, p53 is related to UV-independent pathological pigmentation. In the process of identifying the causative gene of dyschromatosis universalis hereditaria (DUH), three mutations encoding amino acid substitutions were found in the gene SAM and SH3 domain containing 1 (SASH1). SASH1 was identified to interact with guanine nucleotide-binding protein subunit-alpha isoforms short (Gαs). However, for about 90 years, the pathological gene and the pathological mechanism of DUH are unclear. Our study indicates that SASH1 is physiologically medicated by p53 upon UV stimulation and a reciprocal SASH-p53 inducement is existed physiologically and pathophysiologically. A novel p53/POMC/α-MSH/Gαs/SASH1 signal cascade regulates SASH1 to foster melanogenesis. SASH1 mutations control a novel p53/POMC/Gαs/SASH1 autoregulatory positive feedback loop to promote pathological hyperpigmentation phenotype in DUH-affected individuals. Our work illustrates a novel p53/POMC/Gαs/SASH1 autoregulatory positive feedback loop that is mediated by SASH1 mutations to foster pathological hyperpigmentation phenotype
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