手話通訳資格保持者における通訳活動の実態と資質・能力に関する調査研究

本研究では、全国の手話通訳士及び手話通訳者を対象としたWeb 調査を実施し、手話通訳士及び手話通訳者における通訳活動の現状（検討１）と、資質・能力の実態（検討２）について分析・検討した。検討１では、対象者の属性、所持資格に関する情報、通訳活動の実態から、通訳活動に従事する通訳者の特徴について分析・検討した。483名の回答を分析した結果、年齢、手話通訳士資格の有無、資格取得前の経験が、通訳派遣の従事時間や通訳業務に係る雇用の有無と関連することが示されたが、資格取得後の経験年数との関連は明確でなかった。また、地域によって、通訳ニーズや雇用実態が異なることが示唆された。検討２では、職業倫理や行動規範に関する自己評定を求めるとともに、手話通訳スキルのテストを実施した。分析の結果、手話通訳士資格の有無と手話通訳スキルに一定の関係があること、一部の地域を除き手話通訳スキルに顕著な差は認められないこと、手話通訳スキルの高い通訳者においても通訳能力の自己評価が高くないことが明らかとなった。以上を踏まえ、手話通訳に関する通訳者養成に向けた課題や問題点について考察した。In this study, we conducted a nationwide web-based survey of sign language interpreters. In Study 1, to examine the characteristics of sign language interpreters, we analyzed the responses of 483 qualified sign language interpreters regarding (1) individual attributes, (2) sign language interpreting qualifications, and (3) actual status of interpreting activities. The results indicated that age; possessing qualifications recognized by the Ministry of Health, Labor and Welfare; and years of experience prior to gaining qualifications were related to the time spent engaged in interpreting dispatch and to whether the respondent was employed in interpreting-related work. However, the relationship with years of experience after qualifications was unclear. It was also suggested that the demand for and employment status of interpreters varied by region. In Study 2, to examine the characteristics of interpreting skills and related factors, we analyzed (1) the professional ethics of sign language interpreters and (2) sign language interpreting skills. The analysis revealed that there is a relationship between sign language interpreting skills and qualifications. There is no significant difference in sign language interpreting skills, except in some regions. Finally, interpreters with high sign language interpreting skills do not have high self-evaluations of their interpreting competency. The study concludes with a discussion of the issues in training interpreters for sign language interpreting.本研究は、令和３年度厚生労働科学研究費補助金（障害者政策総合研究事業）（20GC1014）の助成を受けた

Development of the h-BN manufacturing process for3D-LSI

Hexagonal-BN (h-BN) based SOI structure with through silicon via (TSV) shows higher heat dissipation performance without degrading electrical characteristics compared with the conventional SOI structure. This paper evaluates the manufacturing process for 3D-LSI concluding h-BN. Hexagonal-BN etched by F2+ He shows useful top shapes of TSV for the 3D-LSI.10th IEEE CPMT Symposium Japan (ICSJ2021), November 10-12, 2021, Kyoto University (A Hybrid Event of On-site and Virtual Meetings

Lattice-matched HfN buffer layers for epitaxy of GaN on Si

Gallium nitride is grown by plasma-assisted molecular-beam epitaxy on (111) and (001) silicon substrates using sputter-deposited hafnium nitride buffer layers. Wurtzite GaN epitaxial layers are obtained on both the (111) and (001) HfN/Si surfaces, with crack-free thickness up to 1.2 (mu)m. Initial results for GaN grown on the (111) surface show a photoluminescence peak width of 17 meV at 11 K, and an asymmetric x-ray rocking curve width of 20 arcmin. Wurtzite GaN on HfN/Si(001) shows reduced structural quality and peculiar low-temperature luminescence features. However, growth on the (001) surface results in nearly stress-free films, suggesting that much thicker crack-free layers could be obtained

Lattice-matched HfN buffer layers for epitaxy of GaN on Si

Gallium nitride is grown by plasma-assisted molecular-beam epitaxy on (111) and (001) silicon substrates using sputter-deposited hafnium nitride buffer layers. Wurtzite GaN epitaxial layers are obtained on both the (111) and (001) HfN/Si surfaces, with crack-free thickness up to 1.2 (mu)m. Initial results for GaN grown on the (111) surface show a photoluminescence peak width of 17 meV at 11 K, and an asymmetric x-ray rocking curve width of 20 arcmin. Wurtzite GaN on HfN/Si(001) shows reduced structural quality and peculiar low-temperature luminescence features. However, growth on the (001) surface results in nearly stress-free films, suggesting that much thicker crack-free layers could be obtained

Epigenetic plasticity safeguards heterochromatin configuration in mammals

Heterochromatin is a key architectural feature of eukaryotic chromosomes critical for cell type-specific gene expression and genome stability. In the mammalian nucleus, heterochromatin segregates from transcriptionally active genomic regions and exists in large, condensed, and inactive nuclear compartments. However, the mechanisms underlying the spatial organization of heterochromatin need to be better understood. Histone H3 lysine 9 trimethylation (H3K9me3) and lysine 27 trimethylation (H3K27me3) are two major epigenetic modifications that enrich constitutive and facultative heterochromatin, respectively. Mammals have at least five H3K9 methyltransferases (SUV39H1, SUV39H2, SETDB1, G9a and GLP) and two H3K27 methyltransferases (EZH1 and EZH2). In this study, we addressed the role of H3K9 and H3K27 methylation in heterochromatin organization using a combination of mutant cells for five H3K9 methyltransferases and an EZH1/2 dual inhibitor, DS3201. We showed that H3K27me3, which is normally segregated from H3K9me3, was redistributed to regions targeted by H3K9me3 after the loss of H3K9 methylation and that the loss of both H3K9 and H3K27 methylation resulted in impaired condensation and spatial organization of heterochromatin. Our data demonstrate that the H3K27me3 pathway safeguards heterochromatin organization after the loss of H3K9 methylation in mammalian cells

A novel NONO variant that causes developmental delay and cardiac phenotypes

Abstract The Drosophila behavior/human splicing protein family is involved in numerous steps of gene regulation. In humans, this family consists of three proteins: SFPQ, PSPC1, and NONO. Hemizygous loss-of-function (LoF) variants in NONO cause a developmental delay with several complications (e.g., distinctive facial features, cardiac symptoms, and skeletal symptoms) in an X-linked recessive manner. Most of the reported variants have been LoF variants, and two missense variants have been reported as likely deleterious but with no functional validation. We report three individuals from two families harboring an identical missense variant that is located in the nuclear localization signal, NONO: NM_001145408.2:c.1375C > G p.(Pro459Ala). All of them were male and the variant was inherited from their asymptomatic mothers. Individual 1 was diagnosed with developmental delay and cardiac phenotypes (ventricular tachycardia and dilated cardiomyopathy), which overlapped with the features of reported individuals having NONO LoF variants. Individuals 2 and 3 were monozygotic twins. Unlike in Individual 1, developmental delay with autistic features was the only symptom found in them. A fly experiment and cell localization experiment showed that the NONO variant impaired its proper intranuclear localization, leading to mild LoF. Our findings suggest that deleterious NONO missense variants should be taken into consideration when whole-exome sequencing is performed on male individuals with developmental delay with or without cardiac symptoms