The Effects of Switching to On-Demand on Learning Outcomes in First-Year PBL Courses

本研究では，対面授業とオンデマンド授業の違いが，初年次PBL科目における学習成果の違いに与える影響を検討した。分析の結果，オンデマンド授業において協同作業認識尺度における協同効用のスコアが対面授業より高い傾向がみられた一方で，協同作業をネガティブに評価する尺度である互恵懸念のスコアが対面授業より低い傾向がみられた。加えて，学習成果全体を観察した場合，オンデマンド授業において，授業に適応的でない学生数が減少し適応的な学生数が増加するという改善がみられた。In this study, we examined the effect of the difference between face-to-face and on-demand classes on the differences in learning outcomes in first-year PBL courses. As a result, it was found that the score of the usefulness of cooperation in the belief in cooperation scale tended to be higher in the on-demand class than in the face-to-face class, while the score of inequity, which is a scale to evaluate collaborative work negatively, tended to be lower in the on-demand class than in the face-to-face class. In addition, when observing the overall learning outcomes, the number of students who were not adaptive to the class decreased and the number of adaptive students increased in the on-demand class

IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression

Background: IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods: IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined. Results: IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs. Conclusions: These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression

Discovery of a Human Neuromedin U Receptor 1‑Selective Hexapeptide Agonist with Enhanced Serum Stability

Neuromedin U (NMU) activates two NMU receptors (NMUR1 and NMUR2) and is a useful antiobesity drug lead. We report discovery of a hexapeptide agonist, 2-thienylacetyl-Trp¹-Phe­(4-F)²-Arg³-Pro⁴-Arg⁵-Asn⁶-NH₂ (<b>4</b>). However, the NMUR1 selectivity and serum stability of this agonist were unsatisfactory. Through a structure–activity relationship study focused on residue 2 of agonist <b>4</b>, serum stability, and pharmacokinetic properties, we report here the discovery of a novel NMUR1 selective hexapeptide agonist <b>7b</b> that suppresses body weight gain in mice

Discovery of a Human Neuromedin U Receptor 1‑Selective Hexapeptide Agonist with Enhanced Serum Stability

Neuromedin U (NMU) activates two NMU receptors (NMUR1 and NMUR2) and is a useful antiobesity drug lead. We report discovery of a hexapeptide agonist, 2-thienylacetyl-Trp¹-Phe­(4-F)²-Arg³-Pro⁴-Arg⁵-Asn⁶-NH₂ (<b>4</b>). However, the NMUR1 selectivity and serum stability of this agonist were unsatisfactory. Through a structure–activity relationship study focused on residue 2 of agonist <b>4</b>, serum stability, and pharmacokinetic properties, we report here the discovery of a novel NMUR1 selective hexapeptide agonist <b>7b</b> that suppresses body weight gain in mice