Distributions of self-trapped hole continuums in silica glass

Photobleaching of self-trapped holes (STH) in low temperature UV-irradiated silica glass has been investigated by the electron spin resonance method. The bleaching time dependence of the decay of two kinds of STH, STH1, and STH2, could be well fitted by the stretched exponential function, and STH2 has a quicker decay than STH1. On the other hand, the decay becomes significant large when the photon energy increases from 1.5to2.0eV, and then keeps constant with a further increase of photon energy. The distributions of the STH continuums are estimated at the positions on top of the valence band, being 1.66±0.27eV for STH1 and 1.63±0.33eV for STH2. A possible recombination mechanism is proposed to explain the decay of STH signals

Fluorine-doping concentration and fictive temperature dependence of self-trapped holes in SiO[sub 2] glasses

Fictive temperature (Tf) and fluorine (F)-doping concentration dependences of self-trapped holes (STHs) in silicaglasses created by UVirradiation at low temperatures have been studied by the electron-paramagnetic-resonance method. It was found that the yield of STH decreases with decreasing Tf and increasing F-doping concentration. In combination with infrared spectra measurements, the correlation among Tf, F-doping concentration, Si–O bond length, and Si–O–Si bond angle was elucidated. We conclude that the change in both Tf and F doping can modify the network of SiO₂glass, leading to the suppression of the formation of STHs

Effect of structural defects on anomalous ultrasound propagation in solids during second-order phase transitions

The effect of structural defects on the critical ultrasound attenuation and ultrasound velocity dispersion in Ising-like three-dimensional systems is studied. A field-theoretical description of the dynamic effects of acoustic-wave propagation in solids during phase transitions is performed with allowance for both fluctuation and relaxation attenuation mechanisms. The temperature and frequency dependences of the scaling functions of the attenuation coefficient and the ultrasound velocity dispersion are calculated in a two-loop approximation for pure and structurally disordered systems, and their asymptotic behavior in hydrodynamic and critical regions is separated. As compared to a pure system, the presence of structural defects in it is shown to cause a stronger increase in the sound attenuation coefficient and the sound velocity dispersion even in the hydrodynamic region as the critical temperature is reached. As compared to pure analogs, structurally disordered systems should exhibit stronger temperature and frequency dependences of the acoustic characteristics in the critical region.Comment: 7 RevTeX pages, 4 figure

Genome and Transcriptome Analysis of the Food-Yeast Candida utilis

The industrially important food-yeast Candida utilis is a Crabtree effect-negative yeast used to produce valuable chemicals and recombinant proteins. In the present study, we conducted whole genome sequencing and phylogenetic analysis of C. utilis, which showed that this yeast diverged long before the formation of the CUG and Saccharomyces/Kluyveromyces clades. In addition, we performed comparative genome and transcriptome analyses using next-generation sequencing, which resulted in the identification of genes important for characteristic phenotypes of C. utilis such as those involved in nitrate assimilation, in addition to the gene encoding the functional hexose transporter. We also found that an antisense transcript of the alcohol dehydrogenase gene, which in silico analysis did not predict to be a functional gene, was transcribed in the stationary-phase, suggesting a novel system of repression of ethanol production. These findings should facilitate the development of more sophisticated systems for the production of useful reagents using C. utilis

Tumor-promoting functions of transforming growth factor-β in progression of cancer

Transforming growth factor-β (TGF-β) elicits both tumor-suppressive and tumor-promoting functions during cancer progression. Here, we describe the tumor-promoting functions of TGF-β and how these functions play a role in cancer progression. Normal epithelial cells undergo epithelial-mesenchymal transition (EMT) through the action of TGF-β, while treatment with TGF-β and fibroblast growth factor (FGF)-2 results in transdifferentiation into activated fibroblastic cells that are highly migratory, thereby facilitating cancer invasion and metastasis. TGF-β also induces EMT in tumor cells, which can be regulated by oncogenic and anti-oncogenic signals. In addition to EMT promotion, invasion and metastasis of cancer are facilitated by TGF-β through other mechanisms, such as regulation of cell survival, angiogenesis, and vascular integrity, and interaction with the tumor microenvironment. TGF-β also plays a critical role in regulating the cancer-initiating properties of certain types of cells, including glioma-initiating cells. These findings thus may be useful for establishing treatment strategies for advanced cancer by inhibiting TGF-β signaling

HLA-B-associated transcript 3 (Bat3/Scythe) negatively regulates Smad phosphorylation in BMP signaling

Members of the transforming growth factor-β (TGF-β) superfamily participate in numerous biological phenomena in multiple tissues, including in cell proliferation, differentiation, and migration. TGF-β superfamily proteins therefore have prominent roles in wound healing, fibrosis, bone formation, and carcinogenesis. However, the molecular mechanisms regulating these signaling pathways are not fully understood. Here, we describe the regulation of bone morphogenic protein (BMP) signaling by Bat3 (also known as Scythe or BAG6). Bat3 overexpression in murine cell lines suppresses the activity of the Id1 promoter normally induced by BMP signaling. Conversely, Bat3 inactivation enhances the induction of direct BMP target genes, such as Id1, Smad6, and Smad7. Consequently, Bat3 deficiency accelerates the differentiation of primary osteoblasts into bone, with a concomitant increase in the bone differentiation markers Runx2, Osterix, and alkaline phosphatase. Using biochemical and cell biological analyses, we show that Bat3 inactivation sustains the C-terminal phosphorylation and nuclear localization of Smad1, 5, and 8 (Smad1/5/8), thereby enhancing biological responses to BMP treatment. At the mechanistic level, we show that Bat3 interacts with the nuclear phosphatase small C-terminal domain phosphatase (SCP) 2, which terminates BMP signaling by dephosphorylating Smad1/5/8. Notably, Bat3 enhances SCP2–Smad1 interaction only when the BMP signaling pathway is activated. Our results demonstrate that Bat3 is an important regulator of BMP signaling that functions by modulating SCP2–Smad interaction