On the optical properties of Ag^{+15} ion-beam irradiated TiO_{2} and SnO_{2} thin films

The effects of 200-MeV Ag^{+15} ion irradiation on the optical properties of TiO_{2} and SnO_{2} thin films prepared by using the RF magnetron sputtering technique were investigated. These films were characterized by using UV-vis spectroscopy, and with increasing irradiation fluence, the transmittance for the TiO_{2} films was observed to increase systematically while that for SnO_{2} was observed to decrease. Absorption spectra of the irradiated samples showed minor changes in the indirect bandgap from 3.44 to 3.59 eV with increasing irradiation fluence for TiO_{2} while significant changes in the direct bandgap from 3.92 to 3.6 eV were observed for SnO_{2}. The observed modifications in the optical properties of both the TiO_{2} and the SnO_{2} systems with irradiation can be attributed to controlled structural disorder/defects in the system.Comment: 6 pages, ICAMD-201

Resolved quadrupolar transition in TiO2

We report an investigation of the direct forbidden absorption edge of TiO2. For the first time we have resolved the weak quadrupolar 1s exciton and measured its binding energy. Taking into account polaron effects, we estimated the bare electron effective mass in the Γ1 minimum of the conduction band and obtained a fairly reasonable value of 3m0

Characterization of TiO2 nanoparticles in langmuir-blodgett films

In this work we have synthesized TiO2 nanoparticles, using either a sol–gel base catalysed process in the interior of CTAB reversed micelles (TiO2 CTAB sol), or the neutralization of a TiO2/H2SO4 solution in the interior of AOT reversed micelles. From the absorption and emission data of the TiO2 nanoparticles it is possible to conclude that in the sol–gel route there remains alkoxide groups in the structure, originating transitions lower than the energy gap of TiO2 semiconductor. These transitions disappear in the neutralization procedure, where the alkoxide groups are absent in the structure. We have assigned the observed indirect and direct optical transitions according to the anatase band structure. TiO2 Langmuir-Blodgett (LB) films were prepared either by direct deposition of titanium isopropoxide or by deposition of the TiO2 CTAB sol. These films showed photoluminescence, which was attributed to band-gap emission and to surface recombination of defect states

Informal One-Sided Target Zone Model and the Swiss Franc

This paper develops a new theoretical model with an asymmetric informal one-sided exchange rate target zone, with an application to the Swiss franc following the removal of the minimum exchange rate of CHF 1.20 per euro in January 2015. We extend and generalize a standard target zone model by introducing perceived uncertainty about the lower edge of the band. We find that informal soft edge target zone bands lead to weaker honeymoon effects, wider target zone ranges, and higher exchange rate volatility than formal target zone bands. These results suggest that it would be beneficial for exchange rate policy intentions to be stated clearly in order to anchor exchange rate expectations and reduce exchange rate volatility. We also study how exchange rate dynamics can be characterized in models in which financial markets are aware of occasional changes in the policy regime. We show that expected changes in the central bank's exchange rate policy may lead to exchange rate oscillations, providing an additional source of exchange rate volatility, and to capture this it is important to take into account the possibility of regime changes in exchange rate policy.</p

Growth behavior of titanium dioxide thin films at different precursor temperatures

The hydrophilic TiO2 films were successfully deposited on slide glass substrates using titanium tetraisopropoxide as a single precursor without carriers or bubbling gases by a metal-organic chemical vapor deposition method. The TiO2 films were employed by scanning electron microscopy, Fourier transform infrared spectrometry, UV-Visible [UV-Vis] spectroscopy, X-ray diffraction, contact angle measurement, and atomic force microscopy. The temperature of the substrate was 500°C, and the temperatures of the precursor were kept at 75°C (sample A) and 60°C (sample B) during the TiO2 film growth. The TiO2 films were characterized by contact angle measurement and UV-Vis spectroscopy. Sample B has a very low contact angle of almost zero due to a superhydrophilic TiO2 surface, and transmittance is 76.85% at the range of 400 to 700 nm, so this condition is very optimal for hydrophilic TiO2 film deposition. However, when the temperature of the precursor is lower than 50°C or higher than 75°C, TiO2 could not be deposited on the substrate and a cloudy TiO2 film was formed due to the increase of surface roughness, respectively

Targeting of prion-infected lymphoid cells to the central nervous system accelerates prion infection

BACKGROUND: Prions, composed of a misfolded protein designated PrP(Sc), are infectious agents causing fatal neurodegenerative diseases. We have shown previously that, following induction of experimental autoimmune encephalomyelitis, prion-infected mice succumb to disease significantly earlier than controls, concomitant with the deposition of PrP(Sc) aggregates in inflamed white matter areas. In the present work, we asked whether prion disease acceleration by experimental autoimmune encephalomyelitis results from infiltration of viable prion-infected immune cells into the central nervous system. METHODS: C57Bl/6 J mice underwent intraperitoneal inoculation with scrapie brain homogenates and were later induced with experimental autoimmune encephalomyelitis by inoculation of MOG(35-55) in complete Freund's adjuvant supplemented with pertussis toxin. Spleen and lymph node cells from the co-induced animals were reactivated and subsequently injected into naïve mice as viable cells or as cell homogenates. Control groups were infected with viable and homogenized scrapie immune cells only with complete Freund's adjuvant. Prion disease incubation times as well as levels and sites of PrP(Sc) deposition were next evaluated. RESULTS: We first show that acceleration of prion disease by experimental autoimmune encephalomyelitis requires the presence of high levels of spleen PrP(Sc). Next, we present evidence that mice infected with activated prion-experimental autoimmune encephalomyelitis viable cells succumb to prion disease considerably faster than do mice infected with equivalent cell extracts or other controls, concomitant with the deposition of PrP(Sc) aggregates in white matter areas in brains and spinal cords. CONCLUSIONS: Our results indicate that inflammatory targeting of viable prion-infected immune cells to the central nervous system accelerates prion disease propagation. We also show that in the absence of such targeting it is the load of PrP(Sc) in the inoculum that determines the infectivity titers for subsequent transmissions. Both of these conclusions have important clinical implications as related to the risk of prion disease contamination of blood products

Protease-Resistant Prions Selectively Decrease Shadoo Protein

The central event in prion diseases is the conformational conversion of the cellular prion protein (PrPC) into PrPSc, a partially protease-resistant and infectious conformer. However, the mechanism by which PrPSc causes neuronal dysfunction remains poorly understood. Levels of Shadoo (Sho), a protein that resembles the flexibly disordered N-terminal domain of PrPC, were found to be reduced in the brains of mice infected with the RML strain of prions [1], implying that Sho levels may reflect the presence of PrPSc in the brain. To test this hypothesis, we examined levels of Sho during prion infection using a variety of experimental systems. Sho protein levels were decreased in the brains of mice, hamsters, voles, and sheep infected with different natural and experimental prion strains. Furthermore, Sho levels were decreased in the brains of prion-infected, transgenic mice overexpressing Sho and in infected neuroblastoma cells. Time-course experiments revealed that Sho levels were inversely proportional to levels of protease-resistant PrPSc. Membrane anchoring and the N-terminal domain of PrP both influenced the inverse relationship between Sho and PrPSc. Although increased Sho levels had no discernible effect on prion replication in mice, we conclude that Sho is the first non-PrP marker specific for prion disease. Additional studies using this paradigm may provide insight into the cellular pathways and systems subverted by PrPSc during prion disease