Asymptotic properties of GMM estimators of stochastic volatility.

Estimator; Stochastic volatility; Volatility;

Asymptotic Results for GMM Estimators of Stochastic Volatility Models

We derive closed-form expressions for the optimal weighting matrix for GMM estimation of the stochastic volatility model with AR(1) log-volatility, and for the asymptotic covariance matrix of the resulting estimator. The moment conditions considered are generated by the absolute observations (which is the standard approach in this literature) or by the log-squared observations. We use the expressions to compare the performances of GMM and other estimators that have been proposed, and to optimally select small sets of moment conditions from very large sets.Stochastic volatility, GMM

The ubiquitin-editing enzyme A20 controls NK cell homeostasis through regulation of mTOR activity and TNF

The ubiquitin-editing enzyme A20 is a well-known regulator of immune cell function and homeostasis. In addition, A20 protects cells from death in an ill-defined manner. While most studies focus on its role in the TNF-receptor complex, we here identify a novel component in the A20-mediated decision between life and death. Loss of A20 in NK cells led to spontaneous NK cell death and severe NK cell lymphopenia. The few remaining NK cells showed an immature, hyperactivated phenotype, hallmarked by the basal release of cytokines and cytotoxic molecules. NK-A20(-/-) cells were hypersensitive to TNF-induced cell death and could be rescued, at least partially, by a combined deficiency with TNF. Unexpectedly, rapamycin, a well-established inhibitor of mTOR, also strongly protected NK-A20(-/-) cells from death, and further studies revealed that A20 restricts mTOR activation in NK cells. This study therefore maps A20 as a crucial regulator of mTOR signaling and underscores the need for a tightly balanced mTOR pathway in NK cell homeostasis

The ubiquitin-editing enzyme A20 controls NK cell homeostasis through regulation of mTOR activity and TNF

The ubiquitin-editing enzyme A20 is a well-known regulator of immune cell function and homeostasis. In addition, A20 protects cells from death in an ill-defined manner. While most studies focus on its role in the TNF-receptor complex, we here identify a novel component in the A20-mediated decision between life and death. Loss of A20 in NK cells led to spontaneous NK cell death and severe NK cell lymphopenia. The few remaining NK cells showed an immature, hyperactivated phenotype, hallmarked by the basal release of cytokines and cytotoxic molecules. NK-A20−/− cells were hypersensitive to TNF-induced cell death and could be rescued, at least partially, by a combined deficiency with TNF. Unexpectedly, rapamycin, a wellestablished inhibitor of mTOR, also strongly protected NK-A20−/− cells from death, and further studies revealed that A20 restricts mTOR activation in NK cells. This study therefore maps A20 as a crucial regulator of mTOR signaling and underscores the need for a tightly balanced mTOR pathway in NK cell homeostasis

Asymptotic properties of GMM estimators of stochastic volatility

status: publishe

Tenckhoff tunneled peritoneal catheter placement in the palliative treatment of malignant ascites: technical results and overall clinical outcome

To assess the technical and clinical outcome of percutaneous insertion of tunneled peritoneal catheters in the palliative treatment of refractory malignant ascites and to determine the safety and feasibility of intraperitoneal administration of cytotoxic drugs through the tunneled catheter