Experimental characterization of the electronic structure of anatase TiO2: Thermopower modulation

Thermopower (S) for anatase TiO2 epitaxial films (n3D: 1E17-1E21 /cm3) and the gate voltage (Vg) dependence of S for thin film transistors (TFTs) based on TiO2 films were investigated to clarify the electronic density of states (DOS) around the conduction band bottom. The slope of the |S|-log n3D plots was -20 {\mu}V/K, which is an order magnitude smaller than that of semiconductors (-198 {\mu}V/K), and the |S| values for the TFTs increased with Vg in the low Vg region, suggesting that the extra tail states are hybridized with the original conduction band bottom.Comment: 11 pages, 4 figure

Asset Pricing under Randomized Solvable Diffusions

By employing a randomization procedure on the geometric Brownian motion (GBM) model, we construct our new pricing models with stochastic volatility exhibiting symmetric smiles in the log-forward moneyness, and admitting simple closed-form analytical expressions for European-style option prices. We assume that there are no infinitesimal correlations between the underlying asset prices and their volatility, and the integrated squared volatility processes are random variables with well-known probability density functions. Under some regularity conditions, closed-form expressions are obtained by taking the expectation of option prices under diffusion models over the integrated squared volatility process, which relate to the Bayesian framework in the GBM model studied by Darsinos and Satchell [12]. Surprisingly, the pricing formulas for the novel models presented in this thesis are even simpler than the classical GBM model as they are expressed as elementary analytical functions. The option prices are also obtained numerically in an efficient manner since they only involve one-dimensional integrals of complementary error functions with respect to the variable of integration. We also calibrate to the market data from Coca Cola to compare the performance on the new models and the SABR model

Class A scavenger receptor 1 (MSR1) restricts hepatitis C virus replication by mediating toll-like receptor 3 recognition of viral RNAs produced in neighboring cells

Persistent infections with hepatitis C virus (HCV) may result in life-threatening liver disease, including cirrhosis and cancer, and impose an important burden on human health. Understanding how the virus is capable of achieving persistence in the majority of those infected is thus an important goal. Although HCV has evolved multiple mechanisms to disrupt and block cellular signaling pathways involved in the induction of interferon (IFN) responses, IFN-stimulated gene (ISG) expression is typically prominent in the HCV-infected liver. Here, we show that Toll-like receptor 3 (TLR3) expressed within uninfected hepatocytes is capable of sensing infection in adjacent cells, initiating a local antiviral response that partially restricts HCV replication. We demonstrate that this is dependent upon the expression of class A scavenger receptor type 1 (MSR1). MSR1 binds extracellular dsRNA, mediating its endocytosis and transport toward the endosome where it is engaged by TLR3, thereby triggering IFN responses in both infected and uninfected cells. RNAi-mediated knockdown of MSR1 expression blocks TLR3 sensing of HCV in infected hepatocyte cultures, leading to increased cellular permissiveness to virus infection. Exogenous expression of Myc-MSR1 restores TLR3 signaling in MSR1-depleted cells with subsequent induction of an antiviral state. A series of conserved basic residues within the carboxy-terminus of the collagen superfamily domain of MSR1 are required for binding and transport of dsRNA, and likely facilitate acidification-dependent release of dsRNA at the site of TLR3 expression in the endosome. Our findings reveal MSR1 to be a critical component of a TLR3-mediated pattern recognition receptor response that exerts an antiviral state in both infected and uninfected hepatocytes, thereby limiting the impact of HCV proteins that disrupt IFN signaling in infected cells and restricting the spread of HCV within the liver

Impact of carotid atherosclerosis on long-term mortality in chronic hemodialysis patients

Impact of carotid atherosclerosis on long-term mortality in chronic hemodialysis patients.BackgroundCardiovascular event is the major cause of mortality in patients on maintenance hemodialysis. We prospectively tested the predictive values of atherosclerotic parameters for all-cause and cardiovascular outcomes in 219 hemodialysis patients (age, 58 ± 13 years; time on hemodialysis, 13 ± 7 years; male/female, 144/75).MethodsWe measured blood homocysteine (Hcy), ultrasound carotid artery intima media thickness (IMT) and % aortic wall calcification at L2/3 region [% of calcification index in the abdominal aortic wall (%ACI)] by computed tomography (CT) scan, and followed all patients for 5 years.ResultsDuring the follow-up periods, 54 patients (25%) died, 40 (74%) of them of cardiovascular causes. IMT was significantly higher in patients who expired (0.75 ± 0.02mm) than in those who survived (0.62 ± 0.01mm). IMT was significantly correlated with age (r = 0.47, P < 0.01) and %ACI (r = 0.27, P < 0.01). The survival rate during the observation was significantly lower in the final IMT third (58%) than in the first (90%) and the middle IMT third (80%) (P < 0.01). Multivariate Cox proportional hazards analysis revealed that diabetes and IMT became independent determinants of all-cause and cardiovascular death. Adjusted hazards ratios of all-cause and cardiovascular mortality for an increase of 0.1mm in IMT were 1.31 (95% CI, 1.07 to 1.59) and 1.41 (95% CI, 1.12 to 1.76). In contrast, %ACI at abdominal aorta and blood Hcy did not affect their 5-year mortality.ConclusionThese findings suggested that measurement of carotid artery IMT is useful for predicting long-term mortality in patients receiving maintenance hemodialysis

Rab13 Is Involved in the Entry Step of Hepatitis C Virus Infection

Membrane transport probably participates in the lifecycle of hepatitis C virus (HCV). Rab proteins are essential host factors for HCV RNA replication, but these proteins’ roles in other steps of the HCV lifecycle are not clear. The tight junction (TJ) plays a key role in HCV infection. Rab13 regulates the endocytic recycling of the TJ-associated proteins. Here we investigated whether Rab13 is involved in the HCV entry step. We used HuH-7-derived RSc cells and Li23-derived D7 cells. To evaluate the effect of Rab13 in HCV infection, we transfected the cells with siRNA targeting Rab13 before HCV infection. The down-regulation of Rab13 inhibited HCV infection. The D7 cells had showed a greater inhibitory effect against HCV infection compared to that in the RSc cells by Rab13 knockdown. Next, to evaluate the effect of Rab13 after infection, we inoculated the cells with HCV before transfection of the siRNA. The down-regulation of Rab13 did not show any effects after HCV infection. We further examined whether Rab13 would influence HCV RNA replication by using HCV replicon-harboring cells. The results revealed that Rab13 did not affect the step of HCV RNA replication. These results suggest that Rab13 plays an important role in the step of HCV entry