Examining the reliability and validity of a self-regulated learning strategy scale for undergraduate nursing students and effective factors of self-regulated learning strategies.

BACKGROUND: Self-regulated learning in higher education has increasingly attracted attention in recent years. This study involved a survey of nursing students using an originally developed tool called the Self-regulated Learning Strategy Scale for Undergraduate Nursing Students (SRLSS-NS). OBJECTIVES: We aimed to elucidate factors relating to the promotion of self-regulated learning while confirming the reliability and validity of the novel scale. DESIGN: A cross-sectional survey design was adopted. SETTING: School of Health Science, Faculty of Medicine. PARTICIPANTS: Participants included first- to fourth-year undergraduate nursing students. METHODS: Descriptive statistics were used to ascertain participant characteristics. We confirmed the criterion-related validity of the survey through exploratory factor analysis and Pearson's product-moment coefficient with external criteria. Reliability was calculated using Cronbach's α coefficient. To examine stability, we confirmed the correlation between the first and second surveys. Multiple regression analysis was performed using the SRLSS-NS score as the objective variable and basic attributes/individual factors, learning-related factors, and cognitive factors as explanatory variables. The statistical significance level was defined as 5 %. RESULTS: The scale consisted of 12 items related to three factors-construct validity, internal consistency, and stability-which were confirmed. Regarding factors related to the SRLS of undergraduate nursing students, the SRLSS-NS score was greater for items such as, "I feel that university education gives me confidence in learning" (ß = 0.255, p < 0.001), "I like/find interest in things I am learning" (ß = 0.228, p < 0.001), "I feel that university education teaches me how to learn" (ß = 0.198, p = 0.003), and "Self-esteem as a professional" (ß = 0.143, p = 0.023). CONCLUSION: As more efforts are made to improve undergraduate nursing students' SRLS, the importance of education for increasing confidence, promoting intrinsic motivation, teaching learning methods, and fostering occupational identity is emphasized.

EAAT1 variants associated with glaucoma.

Glaucoma is one of the leading causes of blindness characterized by progressive loss of retinal ganglion cells (RGCs) and their axons. We reported that glutamate/aspartate transporter (GLAST) knockout mice showed progressive RGC loss and optic nerve degeneration that are similar to glaucoma. To explore the possibility that rare variants in the EAAT1 gene (the human homolog of GLAST) cause susceptibility to glaucoma, we performed targeted sequencing of EAAT1 in 440 patients with glaucoma and 450 control subjects. We identified 8 rare variants in 20 out of 440 patients, including 4 synonymous and 4 missense variants located at protein coding regions. One of these rare variants (rs117295512) showed significant association with the risk of glaucoma (OR = 10.44, P = 0.005). Furthermore, the allele frequency for loss-of-function EAAT1 variants, pAla169Gly and pAla329Thr, was 5.5 folds higher in the glaucoma (1.1%) compared with the control cohort (0.2%). These findings suggest that these rare variants may contribute to the pathogenesis of glaucoma and that loss-of-function variants in EAAT1 are present in a small number of patients with glaucoma.

NMDA receptor subunits have different roles in NMDA-induced neurotoxicity in the retina.

BACKGROUND: Loss of retinal ganglion cells (RGCs) is a hallmark of various retinal diseases including glaucoma, retinal ischemia, and diabetic retinopathy. N-methyl-D-aspartate (NMDA)-type glutamate receptor (NMDAR)-mediated excitotoxicity is thought to be an important contributor to RGC death in these diseases. Native NMDARs are heterotetramers that consist of GluN1 and GluN2 subunits, and GluN2 subunits (GluN2A-D) are major determinants of the pharmacological and biophysical properties of NMDARs. All NMDAR subunits are expressed in RGCs in the retina. However, the relative contribution of the different GluN2 subunits to RGC death by excitotoxicity remains unclear. RESULTS: GluN2B- and GluN2D-deficiency protected RGCs from NMDA-induced excitotoxic retinal cell death. Pharmacological inhibition of the GluN2B subunit attenuated RGC loss in glutamate aspartate transporter deficient mice. CONCLUSIONS: Our data suggest that GluN2B- and GluN2D-containing NMDARs play a critical role in NMDA-induced excitotoxic retinal cell death and RGC degeneration in glutamate aspartate transporter deficient mice. Inhibition of GluN2B and GluN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases.