建学の精神の徹底を図る初年次教育の実践と課題 ―ホスピタリティ概論の分析から―

本研究は、2017年度から始まった本学の初年次教育を定着させるとともに、新入生が大学での教育を理解し、建学の精神に代表される理念やディプロマポリシーを自分のものとして捉え、その実現に向けた主体的な学修の基盤を構築するという初年次教育の目標の達成を図ることにある。このためには、彼らの特性をとらえるとともに、彼らが初年次教育をどのように捉え、理解したかを把握しなければならない。そこで初年次教育の科目の一つとして開設された「ホスピタリティ概論」を活用して、全受講生を対象とした2つの調査を3年間実施した。1つ目の調査は入学当初の学生像をとらえ授業展開に生かすために学生の特徴を把握するものであり、第1回目の授業で実施された。2つ目の調査は授業内容の理解度を評価するものであり、第10回目に実施された。これらの回答を年度と学科毎に集計、分析した。その結果、次のことが明らかになった。①オープンキャンパスへの参加や進学希望状況などの本学入学に至る経緯が学科によって異なること、そして、入学当初には心身に不安を抱いている学生が、どの学科にも相当数存在すること。3年間の調査によって各学科の学生の特色が明らかになり、学科毎の適切な学修支援方策の作成に向けた示唆が得られたこと。②この講義を受けて、建学の精神であるホスピタリティの獲得に大学が力を入れており、その実現が求められていると多くの学生が認識していること、及び、本科目の重点目標である多様性の理解力の育成につながる他学科の学生とのコミュニケーションの機会に意義を見出していること等から、授業の目標達成に向けた順調な歩みが見られること。これらの結果及び他の科目の報告から、初年次教育が定着しつつあること、そして、その目標達成に向けた歩みが順調であると判断した。ただ、更なる充実のための課題も浮かび上がっている

遠隔教育の実施と大学での教育に関する一考察 ―建学の精神を伝える授業のオンラインでの実施をもとに―

2019年末に端を発した新型コロナ感染症（COVID-19）の拡大によって、多くの大学は2020年度の新学期から遠隔教育の実施に踏み切った。本学においても遠隔教育の採用が決定され、ホスピタリティ概論も IT 機器を活用したオンラインでの実施となった。この中で大学教育の将来像に大きな影響を与えると考えられるオンライン授業の在り方を探る基礎調査を実施した。その結果、次のことが明らかになった。1）受講生の IT 環境の整備には、差がみられること、2）受講生の使用する機器は、パソコン、タブレット、スマートフォンに分かれること、3）オンライン授業に関しては、肯定する意見がある一方、改善を要望する意見も見られること、4）スマートフォンのみでの受講者とパソコンおよびタブレットでの受講者を比較分析した結果、画面の明瞭度や授業の進行、及び授業の理解などにおいて両者に差がみられ、スマートフォンのみでの受講者の方が有意に低い結果であったこと、5）遠隔授業に関する要望等の中には、遠隔教育の利点を述べている受講生の他に、授業以外の大学が持つ機能、つまり、友人獲得や相互啓発に関する不安も多くみられたこと。この結果等を踏まえ、オンライン授業のあり方、及び、将来社会における大学教育のあり方に関する提案を行った

Identification and Functional Evaluation of Polyphenols That Induce Regulatory T Cells

Regulatory T cells (Tregs) and CD4(+)/CD25(+) T cells play an important role in the suppression of excessive immune responses, homeostasis of immune function, and oral tolerance. In this study, we screened for food-derived polyphenols that induce Tregs in response to retinaldehyde dehydrogenase (RALDH2) activation using macrophage-like THP-1 cells. THP-1 cells were transfected with an EGFP reporter vector whose expression is regulated under the control of mouse Raldh2 promoter and named THP-1 (Raldh2p-EGFP) cells. The THP-1 (Raldh2p-EGFP) cells were treated with 33 polyphenols after inducing their differentiation into macrophage-like cells using phorbol 12-myristate 13-acetate. Of the 33 polyphenols, five (kaempferol, quercetin, morin, luteolin and fisetin) activated Raldh2 promoter activity, and both quercetin and luteolin activated the endogenous Raldh2 mRNA expression and enzymatic activity. Furthermore, these two polyphenols increased transforming growth factor beta 1 and forkhead box P3 mRNA expression, suggesting that they have Treg-inducing ability. Finally, we verified that these polyphenols could induce Tregs in vivo and consequently induce IgA production. Oral administration of quercetin and luteolin increased IgA production in feces of mice. Therefore, quercetin and luteolin can induce Tregs via RALDH2 activation and consequently increase IgA production, suggesting that they can enhance intestinal barrier function

FOXO3a Potentiates hTERT Gene Expression by Activating c-MYC and Extends the Replicative Life-Span of Human Fibroblast

<div><p>In our previous studies, we reported that SIRT1 prevents cellular senescence in human fibroblast, and that SIRT1-induced inhibition of cellular senescence is due to enhanced hTERT gene expression. In this study, we investigate the molecular mechanisms behind SIRT1-induced potentiation of hTERT transcription and show that FOXO3a functions downstream of SIRT1 and prevents the induction of cellular senescence by enhancing hTERT gene expression. Furthermore, we found that FOXO3a-induced potentiation of hTERT gene expression is regulated in a c-MYC/E-box dependent manner. In addition, we found that FOXO3a binds to the novel binding element in the c-MYC promoter, and this interaction activates the transcription of the c-MYC gene. The resulting increase in c-MYC leads to higher levels of c-MYC recruited to the hTERT promoter and, in turn, activates hTERT gene expression. Taken together, this pathway might constitute the molecular basis for the anti-senescence effects of SIRT1 and FOXO3a.</p></div

Identification of c-MYC promoter elements required for FOXO3a-mediated activation.

<p>A, Schematic representation of the human c-MYC promoter (c-MYCpWT) and its derivatives. Two putative FOXO-binding elements are shown, –1 indicates the first 5′-nucleotide from the translation initiation site, and the underlined nucleotides are those mutated for our experiments. B, Identification of elements for FOXO3a-induced activation. Elements responsible for the FOXO3a-induced activation were determined using luciferase reporters that contain a wild-type c-MYC promoter (c-MYCpWT) or a mutant c-MYC promoter (c-MYCpUM, c-MYCpDM, and c-MYCUDM). C, An increased amount of FOXO3a was recruited to the downstream region of c-MYC promoter when HUC-F2 cells were transduced with recombinant retrovirus expressing SIRT1 or FOXO3aTM. The association of FOXO3a with downstream elements of the c-MYC promoter was assessed by the ChIP assay.</p

FOXO3a enhances hTERT transcription.

<p>Transcriptional activation of the hTERT gene by FOXO3a was determined by normalized luciferase activity under the control of the hTERT core promoter (A) and qRT-PCR analysis of hTERT mRNA (B). SIRT1 activates the transcription of the hTERT gene in a FOXO3a-dependent manner. FOXO3a-dependent transcriptional activation of the hTERT gene by SIRT1 was determined by normalized luciferase activity under the control of the hTERT core promoter (C) and qRT-PCR analysis of hTERT mRNA (D) in shRNA-treated HUC-F2 cells with reduced FOXO3a levels.</p

FOXO3a inhibits the onset of replicative senescence in HUC-F2 cells.

<p>A, Effect of SIRT1 on the activity of FOXO3a in HUC-F2 cells. The activity of FOXO family proteins was determined by normalized luciferase activity under the control of DBE, the consensus sequence for the FOXO family proteins. B, Effect of FOXO3a on replicative senescence of HUC-F2 cells. After HUC-F2 cells were transduced with recombinant retrovirus for FOXO3aWT (○), FOXO3aTM (•), or mock (▵), replicative potential (B) and SA-β-Gal activity (C and D) were monitored. E, Relative telomere length. Relative telomere lengths of HUC-F2 cells transduced with FOXO3aWT, FOXO3aTM or mock were determined by qPCR.</p

Schematic representation of FOXO3a-induced activation of hTERT transcription.

<p>FOXO3a, a downstream target molecule of SIRT1, binds to the downstream FOXO binding element (DBE) in the c-MYC promoter and activates the transcription of c-MYC, which results in the increased transcription of hTERT gene in an E-box dependent manner.</p

Molecular mechanism of the FOXO3a-induced activation of hTERT transcription.

<p>(A) c-MYC/E-box dependency of the FOXO3a-induced activation of hTERT transcription was assessed using luciferase reporters containing a wild-type hTERT core promoter (phTERTp-289) or a mutant hTERT core promoter (phTERTp-289EM). (B) c-MYC recruited to the hTERT core promoter was increased when HUC-F2 cells were transduced with recombinant retrovirus that expressed FOXO3aWT or FOXO3aTM. The association of c-MYC with the hTERT core promoter was assessed using a ChIIP assay. (C) FOXO3a enhances the transcriptional activation of c-MYC. GAL4-c-MYC, pFR-Luc, and the FOXO3aTM expression vector were co-transfected into HUC-F2 cells, and the normalized luciferase activity was assessed. (D) FOXO3a-induced histone H4 acetylation at the hTERT core promoter. HUC-F2 cells were transduced with recombinant retrovirus for FOXO3aWT or FOXO3aTM. The ChIP assay was performed to identify the acetylation status of histone H4 at the hTERT promoter. (E, F) The effect of FOXO3a on the transcription of c-MYC was determined by normalized luciferase activity under the control of the c-MYC promoter (E) and by qRT-PCR analysis of c-MYC mRNA (F).</p