Optical properties of O2 − centres in KCl∶NaCl mixed crystals

The optical properties of O₂ ^– centres in KClNaCl mixed crystals were investigated. The timeresolved spectra and the fluorescence decay time are shown. From the measurements of the radiative decay time, the oscillator strength of the absorption,f _ab=0.045, the oscillator strength of the fluorescence,f _fluo=0.019, and the activation energy E=0.22 eV for the O₂ ^– centre in KClNaCl were determined.     

Aging and availability of binocular disparity and pictorial depth cues in 3D graphics contents

Some stereoblind observers do not perceive depth of 3D stimuli that depends on binocular disparity. These individuals, who have no disabilities, comprise over 5% of the general population. In addition, 17–30% of nonstereoblind young and young–middle people do not use disparity information in certain 3D environments, a phenomenon known as pseudo‐stereoblindness. This study aimed to investigate the relationship between aging and the proportion of pseudo‐stereoblindness in the general population. In an experiment, 134 nonstereoblind participants, ranging in age from 17 to 83 years, judged subjective depth of 3D stimuli containing binocular disparity and pictorial depth cues. Results showed that the proportion of pseudo‐stereoblindness among young (17–24 years old) and young–middle aged observers (25–39 years old) was 29%, in both cases. However, the proportion of pseudo‐stereoblind observers increased in older populations: 65% and 82% in the middle (40–54 years old) and senior (55–83 years old) age groups, respectively. These results suggest that a number of people, especially in elderly populations, have trouble perceiving depth from binocular disparity in 3D graphic contents despite their essential ability to use disparity information.     

Oxidation behavior of TiAl coated with a fine-grain Co-30Cr-4Al film

The oxidation behavior of TiAl coupons coated with a fine-grain Co-30Cr-4Al (mass %) film of about 30-m thickness has been studied at 1100–1400 K in a flow of purified oxygen at atmospheric pressure for up to 500 ks. Three oxidation stages were recognized: initial transient, parabolic, and accelerated stages. However, at 1100 K a parabolic stage continues for more than 800 ks. The activation energy for parabolic oxidation agrees with reported values for the oxidation of alumina-former alloys, although the mass gains during the parabolic stages are relatively small at 1200 and 1300 K. Micropores developed mainly at the scale/coating and coating/substrate interfaces as oxidation proceeded. This is attributable to recrystallization of the coating during oxidation and a Kirkendall effect due to preferential diffusion of Co into the substrate. The accelerated oxidation can be explained in terms of the formation of rutile mounds on the scale.     

Optical implementation of visible gray-image morphology with the visual-area-coding technique

We present a novel scheme of visible gray-image morphology with the visual-area-coding technique (VACT). The VACT is a technique of digitized analog-optical computing in which data are converted into visible coded patterns and processed with the visible form. Because the achievable operations in the VACT are identical to those of mathematical morphology, mathematical morphology is adapted to gray-image morphology with the VACT. Computer simulation and optical experiments of the several operations in mathematical morphology verify the correctness of the proposed technique. The processing capacity of the proposed method is estimated in terms of the space-bandwidth product.     

A novel interferon regulatory factor family transcription factor, ICSAT/Pip/LSIRF, that negatively regulates the activity of interferon-regulated genes

We have isolated a novel cDNA clone encoding interferon (IFN) consensus sequence-binding protein in adult T-cell leukemia cell line or activated T cells (ICSAT); this protein is the human homolog of the recently cloned Pip/LSIRF. ICSAT is structurally most closely related to the previously cloned ICSBP, a member of the IFN regulatory factor (IRF) family of proteins that binds to interferon consensus sequences (ICSs) found in many promoters of the IFN-regulated genes. Among T-cell lines investigated, ICSAT was abundantly expressed in human T-cell leukemia virus type 1 (HTLV-1)-infected T cells. When the HTLV-1 tax gene was expressed or phorbol myristake acetate-A23187 stimulation was used, ICSAT expression was induced in Jurkat cells which otherwise do not express ICSAT. When the binding of ICSAT to four different ICSs was tested, the relative differences in binding affinities for those ICSs were determined. To study the functional role of ICSAT, we performed cotransfection experiments with the human embryonal carcinoma cell line N-Tera2. ICSAT was demonstrated to possess repressive function over the gene activation induced by IFN stimulation or by IRF-1 cotransfection. Such repressive function is similar to that seen in IRF-2 or ICSBP. However, we have found that ICSAT has a different repressive effect from that of IRF-2 or ICSBP in some IFN-responsive reporter constructs. These results suggest that a novel mechanism of gene regulation by "differential repression" is used by multiple members of repressor proteins with different repressive effects on the IFN-responsive genes.     

Deep Phenotyping of Superficial Epidermolytic Ichthyosis due to a Recurrent Mutation in KRT2

Superficial epidermolytic ichthyosis (SEI) is an autosomal dominant inherited ichthyosis. SEI is caused by mutations in KRT2 and frequently shows erythroderma and widespread blistering at birth. We report the clinical manifestations of two patients from a Japanese family with SEI caused by a hotspot mutation, p.Glu487Lys, in KRT2. In addition, we summarize previous reports on SEI patients with the identical mutation. One of the two patients had disease onset at the age of 7 months. The other patient’s age of onset is unknown, but it was in childhood. Neither of the two patients showed erythroderma. To perform deep phenotyping, we studied the age of onset and the frequency of erythroderma in 34 reported SEI cases with the p.Glu487Lys mutation, including the present cases. Among the cases with sufficient clinical information, 44.4% of the cases that were due to p.Glu487Lys in KRT2 occurred at birth. Erythroderma was observed in 11.1% of the cases with p.Glu487Lys in KRT2.     

Downregulation of miR-122-5p Activates Glycolysis via PKM2 in Kupffer Cells of Rat and Mouse Models of Non-Alcoholic Steatohepatitis

Non-alcoholic steatohepatitis (NASH) has pathological characteristics similar to those of alcoholic hepatitis, despite the absence of a drinking history. The greatest threat associated with NASH is its progression to cirrhosis and hepatocellular carcinoma. The pathophysiology of NASH is not fully understood to date. In this study, we investigated the pathophysiology of NASH from the perspective of glycolysis and the Warburg effect, with a particular focus on microRNA regulation in liver-specific macrophages, also known as Kupffer cells. We established NASH rat and mouse models and evaluated various parameters including the liver-to-body weight ratio, blood indexes, and histopathology. A quantitative phosphoproteomic analysis of the NASH rat model livers revealed the activation of glycolysis. Western blotting and immunohistochemistry results indicated that the expression of pyruvate kinase muscle 2 (PKM2), a rate-limiting enzyme of glycolysis, was upregulated in the liver tissues of both NASH models. Moreover, increases in PKM2 and p-PKM2 were observed in the early phase of NASH. These observations were partially induced by the downregulation of microRNA122-5p (miR-122-5p) and occurred particularly in the Kupffer cells. Our results suggest that the activation of glycolysis in Kupffer cells during NASH was partially induced by the upregulation of PKM2 via miR-122-5p suppression.     

Microstructure and analysis of oxide scales formed on Cr-Si-Ni compacts in air and H2O-containing atmosphere

The purpose of this study was to characterize the oxide scales formed on various Cr-Si-Ni compacts at 1273 K in air and H₂O-containing atmosphere by TEM. It was found that CrSi₂-(5-20)mass%Ni compacts form double layer scales, consisting of an outer Cr₂O₃ layer and an inner SiO₂ layer. The oxide scale changed from SiO₂- to Cr₂O₃-based scale with an increase in the Ni concentration. However, it was observed that the oxide scale formed in H₂O-containing atmospheres showed local SiO₂ growth into the substrate. This result suggests that the inward oxidant diffusion promotes the local growth of SiO₂ in the H₂O-containing atmospheres.     

Fracture behaviour and numerical study of resistance spot welded joints in high-strength steel sheet

Cross tension tests of resistance spot welded joints with varying nugget diameter were carried out using 980 MPa high strength steel sheet of 1.6 mm thickness. In proportion, as nugget diameter increased from 3√t to 5√t (where t is thickness), cross tension strength (CTS) increased while fracture morphology simultaneously transferred from interface fracture to full plug fracture. In cases of interface fracture, circumferential crack initiation due to separation of the corona bond arose at an early stage of loading. The crack opening process without propagation was recognized until just before fracture and then the crack propagated to the nugget immediately in a brittle manner around CTS. In full plug fracture, main ductile crack initiation from the notch-like part at the end of sheet separation occurred with the sub-crack initiated at an early stage. The ductile crack propagated toward the HAZ and base material to form full plug fracture. The mode I stress intensity factor was considered as a suitable fracture parameter because the circumferential crack behaved pre-crack for brittle fracture in the nugget region at the final stage. Based on the FE analysis, the mode I stress intensity factor was calculated as 116 MPa √m at CTS as fracture toughness for the nugget. With respect to full plug fracture, ductile crack initiation behaviour from the notch-like part was expressed by concentration of equivalent plastic strain. On the assumption that the ductile crack arose in critical value of equivalent plastic strain, the value was calculated as 0.34 by FE analysis. Reasonable interpretation for interface fracture and full plug fracture in the resistance spot welded joint was proposed due to first crack initiation by stress concentration, brittle fracture by using mode I stress intensity factor, and ductile crack initiation by using equivalent plastic strain.     

Oncogenic Mutation BRAF V600E Changes Phenotypic Behavior of THLE-2 Liver Cells through Alteration of Gene Expression

The accumulation of mutations in cancer driver genes, such as tumor suppressors or proto-oncogenes, affects cellular homeostasis. Disturbances in the mechanism controlling proliferation cause significant augmentation of cell growth and division due to the loss of sensitivity to the regulatory signals. Nowadays, an increasing number of cases of liver cancer are observed worldwide. Data provided by the International Cancer Genome Consortium (ICGC) have indicated many alterations within gene sequences, whose roles in tumor development are not well understood. A comprehensive analysis of liver cancer (virus-associated hepatocellular carcinoma) samples has identified new and rare mutations in B-Raf proto-oncogene (BRAF) in Japanese HCC patients, as well as BRAF V600E mutations in French HCC patients. However, their function in liver cancer has never been investigated. Here, using functional analysis and next generation sequencing, we demonstrate the tumorigenic effect of BRAF V600E on hepatocytes (THLE-2 cell line). Moreover, we identified genes such as BMP6, CXCL11, IL1B, TBX21, RSAD2, MMP10, and SERPIND1, which are possibly regulated by the BRAF V600E-mediated, mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway. Through several functional assays, we demonstrate that BRAF L537M, D594A, and E648G mutations alone are not pathogenic in liver cancer. The investigation of genome mutations and the determination of their impact on cellular processes and functions is crucial to unraveling the molecular mechanisms of liver cancer development.