Merton's Model Explaining CDS Spreads - a panel data study of OMX Stockholm traded firms

Credit risk arises in almost all financial activities. One way to hedge and trade risk is to use Credit Default Swaps that act like an insurance against credit events. The value of the CDS is related to the probability of the reference entity defaulting. In this paper we aimed to determine how well the variables implied by the Merton model explain the CDS spread. A panel data study of 16 companies belonging to the OMX Stockholm equity index shows that the variables have limited explanatory power. An increasing stock return is narrowing the credit default swap spread, but the time dummies account for most of the variation

Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation

Abstract Background SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. Methods qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. Results We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. Conclusions This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy

Low WIP1 Expression Accelerates Ovarian Aging by Promoting Follicular Atresia and Primordial Follicle Activation

Our previous study demonstrated that ovarian wild-type P53-induced phosphatase 1 (WIP1) expression decreased with age. We hypothesized that WIP1 activity was related to ovarian aging. The role of WIP1 in regulating ovarian aging and its mechanisms remain to be elucidated. Adult female mice with or without WIP1 inhibitor (GSK2830371) treatment were divided into three groups (Veh, GSK-7.5, GSK-15) to evaluate the effect of WIP1 on ovarian endocrine and reproductive function and the ovarian reserve. In vitro follicle culture and primary granulosa cell culture were applied to explore the mechanisms of WIP1 in regulating follicular development. This study revealed that WIP1 expression in atretic follicle granulosa cells is significantly lower than that in healthy follicles. Inhibiting WIP1 phosphatase activity in mice induced irregular estrous cycles, caused fertility declines, and decreased the ovarian reserve through triggering excessive follicular atresia and primordial follicle activation. Primordial follicle depletion was accelerated via PI3K-AKT-rpS6 signaling pathway activation. In vitro follicle culture experiments revealed that inhibiting WIP1 activity impaired follicular development and oocyte quality. In vitro granulosa cell experiments further indicated that downregulating WIP1 expression promoted granulosa cell death via WIP1-p53-BAX signaling pathway-mediated apoptosis. These findings suggest that appropriate WIP1 expression is essential for healthy follicular development, and decreased WIP1 expression accelerates ovarian aging by promoting follicular atresia and primordial follicle activation

Synthesis and characterization of anatase nanoadsorbent and application in removal of lead, copper and arsenic from water

The existences of lead, copper, and arsenic in water supplies are great concern due to their potential effects on human health. This study demonstrates beneficial adsorptive eliminations of lead, copper, and arsenic from water using anatase nanoadsorbent produced by sol-gel method followed by calcination at 400 degrees C. The structure of the resulting sample and the surface species of anatase nanoadsorbent were determined using X-ray diffraction (XRD), Raman spectroscopy and X-ray photoelectron spectrometer (XPS). The amounts of adsorbed lead and copper by the nanoadsorbent increased with increasing pH, while the adsorbed arsenic species were almost constant with the changes of pH values. The sorption kinetic data of lead, copper, and arsenic followed the pseudo-second-order model. The equilibrium data were modeled with the help of Langmuir, Freundlich, Redlich-Peterson and Sips equations. Based on the values of correlation coefficients (R-2) and the average percent error (APE), the Langmuir isotherm equation was excellently fitted to the experimental data of the lead adsorption with diminutive error while the adsorptions of copper and arsenic were described better with the Freundlich equation. The maximum experimental adsorption uptakes were 31.25 mg/g for lead, 23.74 mg/g for copper, and 16.98 mg/g for arsenic, respectively. From the thermodynamic calculations the favorable Gibbs energies were entropicatty controlled in the case of lead and copper adsorptions while the arsenic uptake was thermodynamically favorable without any entropic or enthalpic limitations. This study is valuable for the quality utilization of drinking water that includes arsenic, copper and lead contamination by using anatase nanoparticles as a nanoadsorbent