Towards an Understanding of the Engagement and Emotional Behaviour of MOOC Students using Sentiment and Semantic Features

Online learning and teaching increased in 2020, driven by the COVID-19 pandemic. As many researchers attempted to understand the impact stress had on the emotional behaviours and academic performance of students, most studies explored these pre- and during-COVID behaviours in the context of brick and mortar institutions transitioning to online delivery. There is an opportunity to compare the experiences of students in the MOOC environment in this period, particularly in terms of the difference of engagement, semantics and sentiment/stress behaviours in 2019 and 2020. In this study, we use a dataset from AdelaideX between this time period to identify the most significant features that impact student outcomes. Where previous machine learning approaches used singular features such as student interaction or sentiment in discussion forum posts, we incorporate three feature categories of engagement, semantics and sentiment/stress in an ensemble model is based on voting and stacked methods to determining the relationship between them and academic performance. From our results, we discover that sentiment/stress played little part in academic performance and was relatively unchanged in online courses in this dataset between 2019 and 2020. We present two individual student cases to further contextualise our findings.

SARS-CoV-2 Diverges from Other Betacoronaviruses in Only Partially Activating the IRE1α/XBP1 Endoplasmic Reticulum Stress Pathway in Human Lung-Derived Cells.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has killed over 6 million individuals worldwide and continues to spread in countries where vaccines are not yet widely available or its citizens are hesitant to become vaccinated. Therefore, it is critical to unravel the molecular mechanisms that allow SARS-CoV-2 and other coronaviruses to infect and overtake the host machinery of human cells. Coronavirus replication triggers endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR), a key host cell pathway widely believed to be essential for viral replication. We examined the master UPR sensor IRE1α kinase/RNase and its downstream transcription factor effector XBP1s, which is processed through an IRE1α-mediated mRNA splicing event, in human lung-derived cells infected with betacoronaviruses. We found that human respiratory coronavirus OC43 (HCoV-OC43), Middle East respiratory syndrome coronavirus (MERS-CoV), and murine coronavirus (MHV) all induce ER stress and strongly trigger the kinase and RNase activities of IRE1α as well as XBP1 splicing. In contrast, SARS-CoV-2 only partially activates IRE1α through autophosphorylation, but its RNase activity fails to splice XBP1. Moreover, while IRE1α was dispensable for replication in human cells for all coronaviruses tested, it was required for maximal expression of genes associated with several key cellular functions, including the interferon signaling pathway, during SARS-CoV-2 infection. Our data suggest that SARS-CoV-2 actively inhibits the RNase of autophosphorylated IRE1α, perhaps as a strategy to eliminate detection by the host immune system. IMPORTANCE SARS-CoV-2 is the third lethal respiratory coronavirus, after MERS-CoV and SARS-CoV, to emerge this century, causing millions of deaths worldwide. Other common coronaviruses such as HCoV-OC43 cause less severe respiratory disease. Thus, it is imperative to understand the similarities and differences among these viruses in how each interacts with host cells. We focused here on the inositol-requiring enzyme 1α (IRE1α) pathway, part of the host unfolded protein response to virus-induced stress. We found that while MERS-CoV and HCoV-OC43 fully activate the IRE1α kinase and RNase activities, SARS-CoV-2 only partially activates IRE1α, promoting its kinase activity but not RNase activity. Based on IRE1α-dependent gene expression changes during infection, we propose that SARS-CoV-2 prevents IRE1α RNase activation as a strategy to limit detection by the host immune system.

Cannabidiol inhibits SARS-CoV-2 replication through induction of the host ER stress and innate immune responses.

The spread of SARS-CoV-2 and ongoing COVID-19 pandemic underscores the need for new treatments. Here we report that cannabidiol (CBD) inhibits infection of SARS-CoV-2 in cells and mice. CBD and its metabolite 7-OH-CBD, but not THC or other congeneric cannabinoids tested, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after viral entry, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription. CBD inhibits SARS-CoV-2 replication in part by up-regulating the host IRE1α RNase endoplasmic reticulum (ER) stress response and interferon signaling pathways. In matched groups of human patients from the National COVID Cohort Collaborative, CBD (100 mg/ml oral solution per medical records) had a significant negative association with positive SARS-CoV-2 tests. This study highlights CBD as a potential preventative agent for early-stage SARS-CoV-2 infection and merits future clinical trials. We caution against use of non-medical formulations including edibles, inhalants or topicals as a preventative or treatment therapy at the present time.

The Development of a Surgical Oncology Center During the COVID-19 Pandemic.

ABSTRACT: Coronavirus disease 2019 (COVID-19) was declared a pandemic by the World Health Organization on March 11, 2020. By mid-March, London had emerged as the epicenter in the United Kingdom, accounting for 45% of the COVID-19-related mortality. A cancer COVID-19-free "cold hub," through National Health Service partnership with independent institutions, was established to maintain a throughput of surgical oncology patients with an accessible triage system for oncologic specialties. The high population density, commuter volume, and rising COVID-19 incidence heightened the challenge of segregating a vulnerable population that was already at high risk for surgical morbidity and mortality.The aim of this review is to report the experience of developing a multicenter COVID-19-free cold hub with the aim of providing safe surgery for surgical oncology patients. We discuss the timeline, structure, and infection control policy and suggest practical points that may guide other health care systems.The surgical oncology hub treated 1542 patients between March 1 and July 1, 2020. There were no cases of COVID-19-related mortality in a 30-day follow-up. Key strategies for the restructuring of the cancer service included the following: (1) formation of an accessible referral pathway, (2) creation and structuring of cold hub hospitals, (3) development of protocols for infection control and preoperative testing, (4) rapid reorganization of services based on initial feedback, and (5) clear communication and leadership.It has been shown that a surgical oncology cold hub with an accessible referral system and an effective system of preoperative screening system can minimize COVID-19 transmission, morbidity, and mortality, in a region with heavy disease prevalence. This structure represents a safe, ethical, and viable system that can be replicated in other health care systems.