看護技術教育においてICTを活用した自己学習促進ツールの学習効果

New study shows that e-learning system "Kyonet" can help whether used for study or classroom. We administered the questionnaire at the end of the first semester. From an analysis of the results of our questionnaire for students. this study shows the following.1. Students utilizes "Kyonet" voluntarily as an on-demand tool. The tool contains: 1) Videos regarding basic nursing skills: Nursing demonstrationsby teachers are shown in the videos and they are delivered on Kyoritsu University\u27s ICT, "Kyonet". They help students to study when they prepare or review. 2) Mini-exams: These are also delivered on "Kyonet".2. Videos content attracts students interest when they prepare to study.3. Mini-exams help students what they\u27ve learned

Atypical cell death and insufficient matrix organization in long-bone growth plates from Tric-b-knockout mice

Abstract TRIC-A and TRIC-B proteins form homotrimeric cation-permeable channels in the endoplasmic reticulum (ER) and nuclear membranes and are thought to contribute to counterionic flux coupled with store Ca2+ release in various cell types. Serious mutations in the TRIC-B (also referred to as TMEM38B) locus cause autosomal recessive osteogenesis imperfecta (OI), which is characterized by insufficient bone mineralization. We have reported that Tric-b-knockout mice can be used as an OI model; Tric-b deficiency deranges ER Ca2+ handling and thus reduces extracellular matrix (ECM) synthesis in osteoblasts, leading to poor mineralization. Here we report irregular cell death and insufficient ECM in long-bone growth plates from Tric-b-knockout embryos. In the knockout growth plate chondrocytes, excess pro-collagen fibers were occasionally accumulated in severely dilated ER elements. Of the major ER stress pathways, activated PERK/eIF2α (PKR-like ER kinase/ eukaryotic initiation factor 2α) signaling seemed to inordinately alter gene expression to induce apoptosis-related proteins including CHOP (CCAAT/enhancer binding protein homologous protein) and caspase 12 in the knockout chondrocytes. Ca2+ imaging detected aberrant Ca2+ handling in the knockout chondrocytes; ER Ca2+ release was impaired, while cytoplasmic Ca2+ level was elevated. Our observations suggest that Tric-b deficiency directs growth plate chondrocytes to pro-apoptotic states by compromising cellular Ca2+-handling and exacerbating ER stress response, leading to impaired ECM synthesis and accidental cell death

Atypical cell death and insufficient matrix organization in long-bone growth plates from Tric-b-knockout mice

TRIC-A and TRIC-B proteins form homotrimeric cation-permeable channels in the endoplasmic reticulum (ER) and nuclear membranes and are thought to contribute to counterionic flux coupled with store Ca²⁺ release in various cell types. Serious mutations in the TRIC-B (also referred to as TMEM38B) locus cause autosomal recessive osteogenesis imperfecta (OI), which is characterized by insufficient bone mineralization. We have reported that Tric-b-knockout mice can be used as an OI model; Tric-b deficiency deranges ER Ca²⁺ handling and thus reduces extracellular matrix (ECM) synthesis in osteoblasts, leading to poor mineralization. Here we report irregular cell death and insufficient ECM in long-bone growth plates from Tric-b-knockout embryos. In the knockout growth plate chondrocytes, excess pro-collagen fibers were occasionally accumulated in severely dilated ER elements. Of the major ER stress pathways, activated PERK/eIF2α (PKR-like ER kinase/ eukaryotic initiation factor 2α) signaling seemed to inordinately alter gene expression to induce apoptosis-related proteins including CHOP (CCAAT/enhancer binding protein homologous protein) and caspase 12 in the knockout chondrocytes. Ca²⁺ imaging detected aberrant Ca²⁺ handling in the knockout chondrocytes; ER Ca²⁺ release was impaired, while cytoplasmic Ca²⁺ level was elevated. Our observations suggest that Tric-b deficiency directs growth plate chondrocytes to pro-apoptotic states by compromising cellular Ca²⁺-handling and exacerbating ER stress response, leading to impaired ECM synthesis and accidental cell death.家族性骨形成不全症に伴う低身長の病態メカニズムを解明 --TRIC-Bチャネル欠損による軟骨細胞の機能不全と細胞死--. 京都大学プレスリリース. 2023-12-21