Career Decision-Making Self-Efficacy of Freshmen and Sophomores at “A” University during the COVID-19 Pandemic

本稿では，コロナ禍におけるA 大学の大学1・2 年生（大学生低学年）の進路選択セルフ・エフィカシーについて議論する。パネル調査の結果，次の2 つのことが示された。（1）COVID-19 によってもたらされた雇用状況に対する不安は，大学1・2 年生の進路選択セルフ・エフィカシーの向上を阻害している。（2）雇用状況の悪化の下でも，大学1・2 年生の女子学生の進路選択セルフ・エフィカシーは高まっていることが示唆された。We discuss career decision-making self-efficacy (CDMSE) of freshmen and sophomores during the COVID-19 Pandemic. A panel survey with questionnaires (two-way ANOVA with replications) was conducted. The following two results were indicated: (1) the anticipation of a downward trend in employment during the COVID-19 Pandemic is preventing freshmen and sophomores from increasing CDMSE, (2) in spite of the downward trend, first year and second year female students have increased CDMSE

Local structure of alkalis in mixed-alkali borate glass to elucidate the origin of mixed-alkali effect

We report the structural analysis of Na+ and Cs+ in sodium cesium borate crystals and glasses using 23Na and 133Cs magic-angle spinning nuclear magnetic resonance (MAS NMR) spectroscopy. The composition dependence of NMR spectra of the borate was similar to that of the silicate: (1) the peak position of cesium borate crystals shifted to upfield for structures with larger Cs+ coordination numbers, (2) the MAS NMR spectra of xNa2O-yCs2O-3B2O3 (x = 0, 0.25, 0.5, 0.75, 1.0, x + y = 1) glass showed that the average coordination number (CN) of both the alkali cations decreases with increasing Cs+/(Na+ + Cs+) ratio. However, the degree of decrement in borates is much smaller than that in silicates. We have considered that the small difference in CN is due to 4-coordinated B, because it is electrically compensated by the alkali metal ions resulting in the restriction of having various coordinations of O to alkali metal

RNA-Seq–based transcriptome analysis of corneal endothelial cells derived from patients with Fuchs endothelial corneal dystrophy

Abstract Fuchs endothelial corneal dystrophy (FECD) is the most common inherited corneal disease. Fibrillar focal excrescences called guttae and corneal edema due to corneal endothelial cell death result in progressive vision loss. Multiple genetic variants have been reported, but the pathogenesis of FECD is not fully understood. In this study, we used RNA-Seq to analyze differential gene expression in the corneal endothelium obtained from patients with FECD. Differential expression analysis of transcriptomic profiles revealed that expression of 2366 genes (1092 upregulated and 1274 downregulated genes) was significantly altered in the corneal endothelium of patients with FECD compared to healthy subjects. Gene ontology analysis demonstrated an enrichment of genes involved in extracellular matrix (ECM) organization, response to oxidative stress, and apoptotic signaling. Several pathway analyses consistently indicated the dysregulation of ECM-associated pathways. Our differential gene expression findings support the previously proposed underlying mechanisms, including oxidative stress and apoptosis of endothelial cells, as well as the phenotypic clinical FECD hallmark of ECM deposits. Further investigation focusing on differentially expressed genes related to these pathways might be beneficial for elucidating mechanisms and developing novel therapies

FUS regulates RAN translation through modulating the G-quadruplex structure of GGGGCC repeat RNA in C9orf72-linked ALS/FTD

Abnormal expansions of GGGGCC repeat sequence in the noncoding region of the C9orf72 gene is the most common cause of familial amyotrophic lateral sclerosis and frontotemporal dementia (C9-ALS/FTD). The expanded repeat sequence is translated into dipeptide repeat proteins (DPRs) by noncanonical repeat-associated non-AUG (RAN) translation. Since DPRs play central roles in the pathogenesis of C9-ALS/FTD, we here investigate the regulatory mechanisms of RAN translation, focusing on the effects of RNA-binding proteins (RBPs) targeting GGGGCC repeat RNAs. Using C9-ALS/FTD model flies, we demonstrated that the ALS/FTD-linked RBP FUS suppresses RAN translation and neurodegeneration in an RNA-binding activity-dependent manner. Moreover, we found that FUS directly binds to and modulates the G-quadruplex structure of GGGGCC repeat RNA as an RNA chaperone, resulting in the suppression of RAN translation in vitro. These results reveal a previously unrecognized regulatory mechanism of RAN translation by G-quadruplex-targeting RBPs, providing therapeutic insights for C9-ALS/FTD and other repeat expansion diseases