Developing a Scale to Measure Sense of Resistance to Azatoi Behavior

The main purpose of the present study is to develop a scale measuring the sense of resistance to azatoi behavior in female Japanese university students. The participants in this study were 114 Japanese female university students and 18 items were rated. First, the factor structure of the Azatoi Behavior Resistance Scale (ABRS) was investigated using exploratory factor analysis. Then, the validity of the structure was examined using confirmatory factor analysis. The result of the analysis showed that the fit indices indicated the best fit for the four-factor model, and the four factors were gesture, physical contact, adjustment, and typical behavior

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

Prediction of RNA secondary structure with pseudoknots using integer programming

<p>Abstract</p> <p>Background</p> <p>RNA secondary structure prediction is one major task in bioinformatics, and various computational methods have been proposed so far. Pseudoknot is one of the typical substructures appearing in several RNAs, and plays an important role in some biological processes. Prediction of RNA secondary structure with pseudoknots is still challenging since the problem is NP-hard when arbitrary pseudoknots are taken into consideration.</p> <p>Results</p> <p>We introduce a new method of predicting RNA secondary structure with pseudoknots based on integer programming. In our formulation, we aim at minimizing the value of the objective function that reflects free energy of a folding structure of an input RNA sequence. We focus on a practical class of pseudoknots by setting constraints appropriately. Experimental results for a set of real RNA sequences show that our proposed method outperforms several existing methods in sensitivity. Furthermore, for a set of sequences of small length, our approach achieved good performance in both sensitivity and specificity.</p> <p>Conclusion</p> <p>Our integer programming-based approach for RNA structure prediction is flexible and extensible.</p

Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation

OBJECTIVES: The objective of this study was to identify the role of reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in inositol hexaphosphate (IP6)-induced metabolic disruption in human leukemia PLB-985 cells. METHODS: PLB-985 and X chromosome linked gp91-phox gene knockout (X-CGD) cells were treated with 5, 10, or 20 mM IP6 for 24 to 72 h. Cell growth was assayed using a highly water-soluble tetrazolium salt. The rate of apoptotic and necrotic cell death was determined with an Annexin V-fluorescein isothiocyanate/propidium iodide kit. The expression of CD11b as a marker of monocytic property and of LC3 as an autophagy marker was tested, using flow cytometry combined with fluorescent antibodies. RESULTS: Treatment with 5 and 10 mM IP6 for 24 h was found to suppress the growth of both cell lines, though the effect was more dramatic in PLB-985 cells. After 6-h treatment with 20 mM IP6, the necrosis rate of PLB-985 cells was significantly greater than that of X-CGD cells. Further, after 72-h treatment with 10 mM IP6, CD11b expression was observed in PLB-985 cells but inhibited in X-CGD cells. Autophagy monitoring after 6-h treatment with 10 mM IP6 revealed that LC3 expression was suppressed in PLB-985 cells, whereas it was somewhat increased in X-CGD cells. CONCLUSIONS: Our results suggest that NADPH oxidase activation mediates IP6-induced metabolic disruption associated with necrosis, differentiation, cell growth, and autophagy in PLB-985 cells