Discovering teacher and student needs in online courses for improving the Learning Management System (LMS) of universities

The COVID-19 pandemic in 2020 caused a shift from traditional classroom learning to online learning in higher education institutions. This rapid environmental change confused teachers and students, due to their inadequate readiness and past experience with online learning. As synchronous learning had been the primary approach for universities, teachers encountered difficulties increasing asynchronous learning experiences for students, which occur in a Learning Management System (LMS). Therefore, it was apparent that LMSs should be further developed to help teachers ensure a high quality of education asynchronously. This thesis investigates challenges that teachers and students faced in online courses, particularly during the pandemic. Thus, an improved workflow with user-interfaces is proposed that could support teachers to enhance work efficiency and asynchronous interactions with students. Ultimately, teacher and student needs are discovered to help with the development of the LMS that could incorporate digital technologies into teaching practices in an asynchronous learning environment. The research adopts service design and user-centred approaches to collect and analyse qualitative data. The qualitative research methods include interviews and observations, and data analysis is conducted by affinity diagram. Moreover, the concept proposal is validated through a focus group with teachers. Hence, three gaps between teachers and students are identified, reflecting thirteen challenges of online learning. Thus, a workflow is designed based on a teaching process which follows the journey of online courses, and four features that need to be improved are suggested including efficiency, flexibility, compatibility, and learnability. The research is expected to impact on future studies about the development of an LMS that could provide students with high quality of asynchronous learning experiences in universities

Genome-scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib-resistant lung cancer.

Erlotinib is highly effective in lung cancer patients with epidermal growth factor receptor (EGFR) mutations. However, despite initial favorable responses, most patients rapidly develop resistance to erlotinib soon after the initial treatment. This study aims to identify new genes and pathways associated with erlotinib resistance mechanisms in order to develop novel therapeutic strategies. Here, we induced knockout (KO) mutations in erlotinib-resistant human lung cancer cells (NCI-H820) using a genome-scale CRISPR-Cas9 sgRNA library to screen for genes involved in erlotinib susceptibility. The spectrum of sgRNAs incorporated among erlotinib-treated cells was substantially different to that of the untreated cells. Gene set analyses showed a significant depletion of \u27cell cycle process\u27 and \u27protein ubiquitination pathway\u27 genes among erlotinib-treated cells. Chemical inhibitors targeting genes in these two pathways, such as nutlin-3 and carfilzomib, increased cancer cell death when combined with erlotinib in both in vitro cell line and in vivo patient-derived xenograft experiments. Therefore, we propose that targeting cell cycle processes or protein ubiquitination pathways are promising treatment strategies for overcoming resistance to EGFR inhibitors in lung cancer

Direct cell-to-cell transfer in stressed tumor microenvironment aggravates tumorigenic or metastatic potential in pancreatic cancer.

Pancreatic cancer exhibits a characteristic tumor microenvironment (TME) due to enhanced fibrosis and hypoxia and is particularly resistant to conventional chemotherapy. However, the molecular mechanisms underlying TME-associated treatment resistance in pancreatic cancer are not fully understood. Here, we developed an in vitro TME mimic system comprising pancreatic cancer cells, fibroblasts and immune cells, and a stress condition, including hypoxia and gemcitabine. Cells with high viability under stress showed evidence of increased direct cell-to-cell transfer of biomolecules. The resulting derivative cells (CD4

Re-thinking Pedagogy and Dis-embodied Interaction for Online Learning and Co-Design

Online courses are a key means for universities to scale up their educational offerings to wider audiences. In 2020, as the COVID-19 pandemic worsened, many such courses that were initially designed to be given in-person, were pushed online. Instructors and their respective institutions, however, had limited knowledge of processes, practices, and tools to design high-quality learning experiences. This paper collects faculty and student experiences from a Nordic university and outlines key challenges for designing high-quality live online learning sessions. It demonstrates that, given the fundamentally different contexts for learning in digital settings, teachers need to rethink their understanding of what is possible, and engage with creative tools and pedagogical practices that support enhanced learning experiences online.Peer reviewe

Augmentation of the RNA m6A reader signature is associated with poor survival by enhancing cell proliferation and EMT across cancer types

Cancer: The role of modifications to RNA Studying the effects of a chemical modification of messenger RNA molecules (mRNA), which carry genetic information from DNA to the cell's protein-making machinery, reveals new insights into the role of these modifications in cancer, suggesting potential therapeutic approaches. Researchers in Seoul, South Korea, led by Joon-Yong An at Korea University and Sung-Yup Cho at Seoul National University investigated the most common modifications of mRNA involving methyl groups (CH3): addition ('writing'), having a regulatory effect on the cell ('reading') or removal ('erasing'). The molecular activities involved in reading the modifications were increased in all 11 types of cancer in cancer-sampling databases and their own patient cohort. Changes in writing and erasing of the modifications varied with cancer type. The proteins that mediate the reading responses to RNA methylation are possible targets for new anti-cancer drugs. N-6-Methyladenosine (m6A) RNA modification plays a critical role in the posttranscriptional regulation of gene expression. Alterations in cellular m6A levels and m6A-related genes have been reported in many cancers, but whether they play oncogenic or tumor-suppressive roles is inconsistent across cancer types. We investigated common features of alterations in m6A modification and m6A-related genes during carcinogenesis by analyzing transcriptome data of 11 solid tumors from The Cancer Genome Atlas database and our in-house gastric cancer cohort. We calculated m6A writer (W), eraser (E), and reader (R) signatures based on corresponding gene expression. Alterations in the W and E signatures varied according to the cancer type, with a strong positive correlation between the W and E signatures in all types. When the patients were divided according to m6A levels estimated by the ratio of the W and E signatures, the prognostic effect of m6A was inconsistent according to the cancer type. The R and especially the R2 signatures (based on the expression of IGF2BPs) were upregulated in all cancers. Patients with a high R2 signature exhibited poor prognosis across types, which was attributed to enrichment of cell cycle- and epithelial-mesenchymal transition-related pathways. Our study demonstrates common features of m6A alterations across cancer types and suggests that targeting m6A R proteins is a promising strategy for cancer treatment.N

Cell-permeable NM23 blocks the maintenance and progression of established pulmonary metastasis

Occult metastases are a major cause of cancer mortality, even among patients undergoing curative resection. Therefore, practical strategies to target the growth and persistence of already established metastases would provide an important advance in cancer treatment. Here, we assessed the potential of protein therapy using a cell permeable NM23-H1 metastasis suppressor protein. Hydrophobic transduction domains developed from a screen of 1,500 signaling peptide sequences enhanced the uptake of the NM23 protein by cultured cells and systemic delivery to animal tissues. The cell-permeable (CP)-NM23 inhibited metastasis-associated phenotypes in tumor cell lines, blocked the establishment of lung metastases, and cleared already established pulmonary metastases, significantly prolonging the survival of tumor-bearing animals. Therefore, these results establish the potential use of cell-permeable metastasis suppressors as adjuvant therapy against disseminated cancers