トクシマ ダイガク コウガクブ ノ コウガク ケイモウ カツドウ ノ シンニュウガクセイ エノ エイキョウ : カガク タイケン フェスティバル in トクシマ エンジニアリング フェスティバル マデ

全国の大学では，工学離れを紡ぐため様々な取り組みを行っているが、その具体的効果の検証を行った例はほとんどない。本論文では，徳島大学工学部が実施している工学啓蒙活動，具体的には，科学体験フェスティパルin徳島(幼児～中学生対象）、工学体験大学講座(高校生対象）オープンキャンパス(高校生対象)，出張講義（高校生対象)およびエンジニアリングフェスティバル（高校生～社会人対象)の工学部新入生への影響をアンケート調査した結果に基づき検証を行った。大学の進路は，大学入試を具体的に考える高等学校在学時に決まるという認識が一般的である。本検証においても，高等学校在籍時に受けた上記の啓蒙活動が，本学工学部への入学に大きな影響を与えていることは認められた。しかしながら，小学校入学前後の比較的低年齢時に受けた啓蒙活動も，徳島大学工学部入学，さらには徳島県から全国への理系進学に大きな影響を与えていることが明らかとなった。In the present paper，the influence of the propagation of engineering-related information on the freshmen in the Faculty by the Faculty of Engineering，The University of Tokushima，through projects such as the "Science Summer Festival in Tokushima"， "Kougaku Taiken Daigaku Kouza (Experiences of the University of Engineering)"，“Open Campus". "Shutcho Kougi (Lecture by Professars of the Faculty at a High School)" and "Engineering Festival" on freshmen in the Faculty has been described. As is generally expected, the familiarizing of the high-school students with the subject of engineering seems to be the most basic objective of the propogation of information on the subject of engineering. However it should be noted that the faculty freshmen have also pointed out an additional advantageous effect of the content of above-mentioned propagation project such as "Science Summer Festival in Tokushima": they have also proved useful in familiarizing pupils wiih the subject of engineering

Omecamtiv mecarbil in chronic heart failure with reduced ejection fraction, GALACTIC‐HF: baseline characteristics and comparison with contemporary clinical trials

Aims: The safety and efficacy of the novel selective cardiac myosin activator, omecamtiv mecarbil, in patients with heart failure with reduced ejection fraction (HFrEF) is tested in the Global Approach to Lowering Adverse Cardiac outcomes Through Improving Contractility in Heart Failure (GALACTIC‐HF) trial. Here we describe the baseline characteristics of participants in GALACTIC‐HF and how these compare with other contemporary trials. Methods and Results: Adults with established HFrEF, New York Heart Association functional class (NYHA) ≥ II, EF ≤35%, elevated natriuretic peptides and either current hospitalization for HF or history of hospitalization/ emergency department visit for HF within a year were randomized to either placebo or omecamtiv mecarbil (pharmacokinetic‐guided dosing: 25, 37.5 or 50 mg bid). 8256 patients [male (79%), non‐white (22%), mean age 65 years] were enrolled with a mean EF 27%, ischemic etiology in 54%, NYHA II 53% and III/IV 47%, and median NT‐proBNP 1971 pg/mL. HF therapies at baseline were among the most effectively employed in contemporary HF trials. GALACTIC‐HF randomized patients representative of recent HF registries and trials with substantial numbers of patients also having characteristics understudied in previous trials including more from North America (n = 1386), enrolled as inpatients (n = 2084), systolic blood pressure < 100 mmHg (n = 1127), estimated glomerular filtration rate < 30 mL/min/1.73 m2 (n = 528), and treated with sacubitril‐valsartan at baseline (n = 1594). Conclusions: GALACTIC‐HF enrolled a well‐treated, high‐risk population from both inpatient and outpatient settings, which will provide a definitive evaluation of the efficacy and safety of this novel therapy, as well as informing its potential future implementation

Epithelial-specific histone modification of the miR-96/182 locus targeting AMAP1 mRNA predisposes p53 to suppress cell invasion in epithelial cells

Background: TP53 mutations in cancer cells often evoke cell invasiveness, whereas fibroblasts show invasiveness in the presence of intact TP53. AMAP1 (also called DDEF1 or ASAP1) is a downstream effector of ARF6 and is essential for the ARF6-driven cell-invasive phenotype. We found that AMAP1 levels are under the control of p53 (TP53 gene product) in epithelial cells but not in fibroblasts, and here addressed that molecular basis of the epithelial-specific function of p53 in suppressing invasiveness via targeting AMAP1. Methods: Using MDA-MB-231 cells expressing wild-type and p53 mutants, we identified miRNAs in which their expression is controlled by normal-p53. Among them, we identified miRNAs that target AMAP1 mRNA, and analyzed their expression levels and epigenetic statuses in epithelial cells and nonepithelial cells. Results: We found that normal-p53 suppresses AMAP1 mRNA in cancer cells and normal epithelial cells, and that more than 30 miRNAs are induced by normal-p53. Among them, miR-96 and miR-182 were found to target the 3′-untranslated region of AMAP1 mRNA. Fibroblasts did not express these miRNAs at detectable levels. The ENCODE dataset demonstrated that the promoter region of the miR-183-96-182 cistron is enriched with H3K27 acetylation in epithelial cells, whereas this locus is enriched with H3K27 trimethylation in fibroblasts and other non-epithelial cells. miRNAs, such as miR-423, which are under the control of p53 but not associated with AMAP1 mRNA, demonstrated similar histone modifications at their gene loci in epithelial cells and fibroblasts, and were expressed in these cells. Conclusion: Histone modifications of certain miRNA loci, such as the miR-183-96-182 cistron, are different between epithelial cells and non-epithelial cells. Such epithelial-specific miRNA regulation appears to provide the molecular basis for the epithelial-specific function of p53 in suppressing ARF6-driven invasiveness