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        Effects of changing from on-site to online distance classes on graduate students’ help-seeking: lessons for sustainable teaching and learning from the COVID-19 pandemic

        Ashida, Akemi,Ishizaka, Hiroki 서울대학교 교육연구소 2022 Asia Pacific Education Review Vol.23 No.4

        Over the past decade, the Japanese government and Japanese universities have increased student mobility, both inbound and outbound, to accelerate the internationalization of higher education. However, student mobility was halted in early 2020 because of the COVID-19 pandemic, and international students who had planned to engage in a traditional study abroad program could not enter Japan. The current study examined whether the unexpected implementation of online distance classes because of the pandemic affected the learning strategies of graduate students, including international students. In addition, we investigated whether the online courses functioned as an alternative to face-to-face classes. An analysis using structural equation modeling revealed that the period of enrollment, self-regulation, and country of residence were factors that influenced help-seeking behavior. Graduate students who had enrolled before the pandemic and already experienced face-to-face classes were more likely to actively seek help from instructors and classmates in online classes. Furthermore, graduate students who were unable to enter the country but were taking classes online also tended to actively engage in help-seeking from their instructors and classmates. Students’ experiences of the sudden change to distance learning suggest that, to ensure a sustainable teaching and learning environment in various contexts, instructors should use class designs that consider distance learning, particularly designs that enhance students’ help-seeking, even under normal circumstances. In addition, ensuring sufficient online/virtual spaces for communication among teachers and students is important.

      • Structural and biochemical basis for the inhibition of cell death by APIP, a methionine salvage enzyme

        Kang, Wonchull,Hong, Se Hoon,Lee, Hye Min,Kim, Na Yeon,Lim, Yun Chan,Le, Le Thi My,Lim, Bitna,Kim, Hyun Chul,Kim, Tae Yeon,Ashida, Hiroki,Yokota, Akiho,Hah, Sang Soo,Chun, Keun Ho,Jung, Yong-Keun,Yang National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.1

        <P>APIP, Apaf-1 interacting protein, has been known to inhibit two main types of programmed cell death, apoptosis and pyroptosis, and was recently found to be associated with cancers and inflammatory diseases. Distinct from its inhibitory role in cell death, APIP was also shown to act as a 5-methylthioribulose-1-phosphate dehydratase, or MtnB, in the methionine salvage pathway. Here we report the structural and enzymatic characterization of human APIP as an MtnB enzyme with a <I>K</I><SUB><I>m</I></SUB> of 9.32 μM and a <I>V</I><SUB><I>max</I></SUB> of 1.39 μmol min<SUP>−1</SUP> mg<SUP>−1</SUP>. The crystal structure was determined at 2.0-Å resolution, revealing an overall fold similar to members of the zinc-dependent class II aldolase family. APIP/MtnB exists as a tetramer in solution and exhibits an assembly with <I>C4</I> symmetry in the crystal lattice. The pocket-shaped active site is located at the end of a long cleft between two adjacent subunits. We propose an enzymatic reaction mechanism involving Glu139* as a catalytic acid/base, as supported by enzymatic assay, substrate-docking study, and sequence conservation analysis. We explored the relationship between two distinct functions of APIP/MtnB, cell death inhibition, and methionine salvage, by measuring the ability of enzymatic mutants to inhibit cell death, and determined that APIP/MtnB functions as a cell death inhibitor independently of its MtnB enzyme activity for apoptosis induced by either hypoxia or etoposide, but dependently for caspase-1-induced pyroptosis. Our results establish the structural and biochemical groundwork for future mechanistic studies of the role of APIP/MtnB in modulating cell death and inflammation and in the development of related diseases.</P>

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