Plasma Nitridation of 4H-SiC by Glow Discharge of N2/H2 Mixed Gases

The mixed gas of nitrogen and hydrogen was used for the plasma nitridation of SiC surface.A small amount of hydrogen was effective to activate the nitridation reaction and suppress the oxidationreaction. The interface properties were improved by using nitride layer as an interfacial bufferlayer of SiC MIS structure.ArticleMaterials Science Forum, Vols. 821-823, pp. 504-507 (2015)journal articl

Preparation and Characterization of Nitridation Layer on 4H SiC (0001) Surface by Direct Plasma Nitridation

A nitride layer was formed on a SiC surface by plasma nitridation using pure nitrogen as the reaction gas at the temperature from 800°C to 1400°C. The surface was characterized by XPS. The XPS measurement showed that an oxinitride layer was formed on the SiC surface by the plasma nitridation. The high process temperature seemed to be effective to activate the niridation reaction. A SiO2 film was deposited on the nitridation layer to form SiO2/nitride/SiC structure. The interface state density of the SiO2/nitride/SiC structure was lower than that of the SiO2/SiC structure. This suggested that the nitridation was effective to improve the interface property.ArticleMaterials Science Forum, Vols. 778-780, pp. 631-634 (2014)journal articl

The Expression Level of HIV-1 Vif Is Optimized by Nucleotide Changes in the Genomic SA1D2prox Region during the Viral Adaptation Process

HIV-1 Vif plays an essential role in viral replication by antagonizing anti-viral cellular restriction factors, a family of APOBEC3 proteins. We have previously shown that naturally-occurring single-nucleotide mutations in the SA1D2prox region, which surrounds the splicing acceptor 1 and splicing donor 2 sites of the HIV-1 genome, dramatically alter the Vif expression level, resulting in variants with low or excessive Vif expression. In this study, we investigated how these HIV-1 variants with poor replication ability adapt and evolve under the pressure of APOBEC3 proteins. Adapted clones obtained through adaptation experiments exhibited an altered replication ability and Vif expression level compared to each parental clone. While various mutations were present throughout the viral genome, all replication-competent adapted clones with altered Vif expression levels were found to bear them within SA1D2prox, without exception. Indeed, the mutations identified within SA1D2prox were responsible for changes in the Vif expression levels and altered the splicing pattern. Moreover, for samples collected from HIV-1-infected patients, we showed that the nucleotide sequences of SA1D2prox can be chronologically changed and concomitantly affect the Vif expression levels. Taken together, these results demonstrated the importance of the SA1D2prox nucleotide sequence for modulating the Vif expression level during HIV-1 replication and adaptation

Factors Associated with Improvement in Activities of Daily Living during Hospitalization: A Retrospective Study of Older Patients with Hip Fractures

Background In this study, we aimed to examine the changes in delirium during hospitalization of patients and its association with behavioral and psychological symptoms of dementia (BPSD), as well as improvements in activities of daily living (ADL). Methods A longitudinal, retrospective cohort study was conducted involving 83 older adults (≥65 years) with hip fractures. We collected Mini-Mental State Examination (MMSE) and Functional Independence Measure-motor domain (m-FIM) assessment results from the medical charts at two time points: baseline (first week of hospitalization) and pre-discharge (final week before discharge). Additionally, we collected data on delirium and BPSD at three points: baseline, week 2 post-admission, and pre-discharge. We performed univariate logistic regression analysis using changes in m-FIM scores as the dependent variable and MMSE and m-FIM scores at baseline and pre-discharge, along with delirium and BPSD subtypes at baseline, week 2 post-admission, and pre-discharge, as the explanatory variables. Finally, we performed a multivariate logistic regression analysis incorporating the significant variables from the univariate analysis to identify factors associated with ADL improvement during hospitalization. Results We observed significant correlations between ADL improvement during hospitalization and baseline m-FIM and MMSE scores, hypoactive delirium state, and BPSD subtype pre-discharge. Notably, all participants with hypoactive symptoms before discharge exhibited some subtype of delirium and BPSD at baseline. Conclusion Besides ADL ability and cognitive function at admission, the presence of hypoactive delirium and BPSD subtype before discharge may hinder ADL improvement during hospitalization

Photocycle features of heterologously expressed and assembled eukaryotic flavin-binding BLUF domains of photoactivated adenylyl cyclase (PAC), a blue-light receptor in Euglena gracilis

Photoactivated adenylyl cyclase (PAC) is a recently discovered blue-light photoreceptor that mediates photomovement in Euglena gracilis (Iseki et al., Nature, 2002, 415, 1047-1051). PAC appears to be a heterotetramer composed of two FAD-binding subunits (PACα and PACβ). Both subunits have a pair of homologous regions (F1 and F2) which show homology with prokaryotic "sensors of blue-light using FAD" (BLUF) domains. The F1 and F2 domains of PAC are the only eukaryotic BLUF domains found thus far. We obtained soluble recombinant F1 and F2 proteins in PACα by heterologous expression with fused glutathione-S-transferase (GST) in E. coli. The expressed F1 samples did not bind flavins, but the F2 samples contained both FAD and FMN with trace amounts of riboflavin. We also assembled the histidine-tagged recombinant F2 (6His-F2) from inclusion bodies in E. coli with exogenous FAD or FMN. Blue-light-induced changes in absorption spectra of these assembled samples were highly similar to those reported for prokaryotic BLUF domains. The FAD- or FMN-assembled 6His-F2 photocycled with nearly the same rate constants of light-reaction and dark-relaxation, which were slightly lower than those of GST-cleaved F2. The estimated quantum efficiency for the phototransformation was 0.28-0.32, and the half-life was 34-44 s at 25 °C for the recombinant PACα F2, whereas that reported for prokaryotic BLUF domains varied from ca. 3.5 s (Tl10078) to ca. 900 s (AppA). The mutated recombinant Y472F and Q514G of PACα F2 and the F2 domain of the PACα homologue from Eutreptiella gymnastica, which lacks the Gln residue conserved in other BLUF domains, showed no photoinduced transformation

Usefulness of a new DUV-LED device for the control of infection by Escherichia coli, Staphylococcus aureus, mycobacteria and spore-forming bacteria

Reliable disinfection and sterilization technologies are needed to deal with the various infectious diseases spreading around the world. Furthermore, bacteria that are difficult to eliminate by ordinary disinfection are also a problem in the medical environment. We examined the germicidal effect of a newly developed deep-ultraviolet light-emitting diode (DUV-LED) prototype device (wavelength of 280 ± 5 nm; power of 0.9 to 1.4 mW/cm2) for floor sterilization against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), Mycobacterium gordonae (M. gordonae), and Bacillus subtilis (B. subtilis). This prototype device is equipped with highly practical DUV-LEDs with a high output efficiency and a long life, and was designed with consideration of the irradiation distance and the angle of the DUV-LEDs to provide a uniform irradiation rate. We found a statistically significant reduction of ≥90% in the infectious titers of both E. coli and S. aureus after irradiation for 2 s. Although acid-fast bacilli and spore-type bacilli are generally thought to be resistant to UV light irradiation compared to general bacteria, the acid-fast bacillus M. gordonae was inactivated after irradiation for 10 s, and spore-type cells of the bacillus B. subtilis were inactivated by ≥90% after irradiation for 30 s. We also found that the effects were cumulative when irradiation was performed at intervals. In the future, the usefulness of this device as an infection control measure will be evaluated in daily medical practice

Tamiflu-Resistant but HA-Mediated Cell-to-Cell Transmission through Apical Membranes of Cell-Associated Influenza Viruses

The infection of viruses to a neighboring cell is considered to be beneficial in terms of evasion from host anti-virus defense systems. There are two pathways for viral infection to “right next door”: one is the virus transmission through cell-cell fusion by forming syncytium without production of progeny virions, and the other is mediated by virions without virus diffusion, generally designated cell-to-cell transmission. Influenza viruses are believed to be transmitted as cell-free virus from infected cells to uninfected cells. Here, we demonstrated that influenza virus can utilize cell-to-cell transmission pathway through apical membranes, by handover of virions on the surface of an infected cell to adjacent host cells. Live cell imaging techniques showed that a recombinant influenza virus, in which the neuraminidase gene was replaced with the green fluorescence protein gene, spreads from an infected cell to adjacent cells forming infected cell clusters. This type of virus spreading requires HA activation by protease treatment. The cell-to-cell transmission was also blocked by amantadine, which inhibits the acidification of endosomes required for uncoating of influenza virus particles in endosomes, indicating that functional hemagglutinin and endosome acidification by M2 ion channel were essential for the cell-to-cell influenza virus transmission. Furthermore, in the cell-to-cell transmission of influenza virus, progeny virions could remain associated with the surface of infected cell even after budding, for the progeny virions to be passed on to adjacent uninfected cells. The evidence that cell-to-cell transmission occurs in influenza virus lead to the caution that local infection proceeds even when treated with neuraminidase inhibitors