A Case Study on Online Learning and Digital Assessment in Times of Crisis

To minimise the adverse impact on student learning due to escalating social unrest started locally in June 2019 and the current COVID-19 pandemic, Hong Kong Baptist University has emphatically strengthened its strategic resolve in e-Learning deployment. With various measures and e-Learning initiatives rolled out, HKBU teachers gained more momentum in launching online classes and conducting e-Assessments with different e-Tools. Peer-sharing from teachers who have successfully implemented online classes and digital assessment was conducive to creating a culture to fast-track e-Learning adoption. This case study sheds light on how virtual teaching and learning have assisted HKBU teachers and students circumvent the recent crises. The study also identifies determining factors and challenges of adopting e-Learning strategies at the University

Gamification for Teamwork Skills: Can a Challenge-based Online Tournament Help Students Learn New Knowledge Collaboratively in Teams?

The interest in deploying innovative technologies with gamification to engage student learning in enjoyable style has been growing. This study aimed to investigate whether a purposely designed eTournament with the integration of concepts of gamification and team development could help the participating tertiary education students (N=416) from a variety of backgrounds in terms of culture and discipline to learn to work in teams collaboratively in a challenge-based online game. The qualitative data collected from the top 10 teams’ online discussions supported that the thoughtful design of the eTournament did facilitate their development of teamwork skills. In addition, quantitative data collected from two of the Post-game Questionnaire questions indicated that over 79% of the respondents strongly agree or agree that they enjoyed the eTournamentin general, and over 84% of respondents strongly agree or agree that they become more aware of the seventeen United Nations Sustainable Development Goals because of the eTournament. Notwithstanding, findings in this study show little evidence in supporting team-playing in PaGamO due to the design of the game regardless of the teamwork skills developed in the early stage of the eTournament. Suggestions to address the limitations of this study are also presented for future improvement

Helping Students to Build Multicultural and Multidisciplinary Competences: A Pilot of Challenge-Based Collaborative Learning on a Digital Gamified Platform

Global issues such as poverty, hunger, and environmental problems are inextricable and cannot be solved comprehensively by homogeneous groups. With the advance of technology, collaborations with peoples at different geographical locations can be achieved effectively. Higher education in the 21st Century must therefore facilitate students to learn how to eclectically connect their creativity and problem-solving skills with technology, and most importantly to work with heterogeneous groups to solve complex global issues.This paper will elaborate on a pilot study of a project in Hong Kong, titled the CCGame Project, which aims to heighten students’ multicultural and multidisciplinary competences by deploying gamified learning and challenge-based learning. Team-based, self-guided learning is the core of the challenge-based learning approach. To preserve students’ interest in learning and accomplishing the tasks for the team, cloud-based learning platforms have been deployed. In the pilot, the online learning platform collected data for analysis of individual and team behaviour. The pilot demonstrated that students could work in a diverse team to complete a challenge. Evidence-based results supported with data analytics will be presented and the project’s plan of work will also be elucidated in this paper

Frataxin deficiency increases cyclooxygenase 2 and prostaglandins in cell and animal models of Friedreich's ataxia

© The Author 2014. Published by Oxford University Press This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.An inherited deficiency of the mitochondrial protein frataxin causes Friedreich's ataxia (FRDA); the mechanism by which this deficiency triggers neuro- and cardio-degeneration is unclear. Microarrays of neural tissue of animal models of the disease showed decreases in antioxidant genes, and increases in inflammatory genes. Cyclooxygenase (COX)-derived oxylipins are important mediators of inflammation. We measured oxylipin levels using tandem mass spectrometry and ELISAs in multiple cell and animal models of FRDA. Mass spectrometry revealed increases in concentrations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar samples of knockin knockout mice. One possible explanation for the elevated oxylipins is that frataxin deficiency results in increased COX activity. While constitutive COX1 was unchanged, inducible COX2 expression was elevated over 1.35-fold (P < 0.05) in two Friedreich's mouse models and Friedreich's lymphocytes. Consistent with higher COX2 expression, its activity was also increased by 58% over controls. COX2 expression is driven by multiple transcription factors, including activator protein 1 and cAMP response element-binding protein, both of which were elevated over 1.52-fold in cerebella. Taken together, the results support the hypothesis that reduced expression of frataxin leads to elevation of COX2-mediated oxylipin synthesis stimulated by increases in transcription factors that respond to increased reactive oxygen species. These findings support a neuroinflammatory mechanism in FRDA, which has both pathomechanistic and therapeutic implications.The study was supported by NIH grants NS077777, EY012245 and AG025532 to G.A.C., and USDA-ARS Intramural Projects 5306-51530-019-00D and 1 U24 DK097154-01 to J.W.N. Funding to pay the Open Access publication charges for this article was provided by the NIH

Seizure-Related Gene 6 (Sez-6) in Amacrine Cells of the Rodent Retina and the Consequence of Gene Deletion

Background: Seizure-related gene 6 (Sez-6) is expressed in neurons of the mouse brain, retina and spinal cord. In the cortex, Sez-6 plays a role in specifying dendritic branching patterns and excitatory synapse numbers during development. Methodology/Principal Findings: The distribution pattern of Sez-6 in the retina was studied using a polyclonal antibody that detects the multiple isoforms of Sez-6. Prominent immunostaining was detected in GABAergic, but not in All glycinergic, amacrine cell subpopulations of the rat and mouse retina. Amacrine cell somata displayed a distinct staining pattern with the Sez-6 antibody: a discrete, often roughly triangular-shaped bright spot positioned between the nucleus and the apical dendrite superimposed over weaker general cytoplasmic staining. Displaced amacrines in the ganglion cell layer were also positive for Sez-6 and weaker staining was occasionally observed in neurons with the morphology of alpha ganglion cells. Two distinct Sez-6 positive strata were present in the inner plexiform layer in addition to generalized punctate staining. Certain inner nuclear layer cells, including bipolar cells, stained more weakly and diffusely than amacrine cells, although some bipolar cells exhibited a perinuclear "bright spot" similar to amacrine cells. In order to assess the role of Sez-6 in the retina, we analyzed the morphology of the Sez-6 knockout mouse retina with immunohistochemical markers and compared ganglion cell dendritic arbor patterning in Sez-6 null retinae with controls. The functional importance of Sez-6 was assessed by dark-adapted paired-flash electroretinography (ERG). Conclusions: In summary, we have reported the detailed expression pattern of a novel retinal marker with broad cell specificity, useful for retinal characterization in rodent experimental models. Retinal morphology, ganglion cell dendritic branching and ERG waveforms appeared normal in the Sez-6 knockout mouse suggesting that, in spite of widespread expression of Sez-6, retinal function in the absence of Sez-6 is not affected

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN