Virtual Wards: A Rapid Adaptation to Clinical Attachments in MBChB During the COVID-19 Pandemic.

When the COVID-19 pandemic suddenly prevented medical students from attending their clinical attachments, the faculty involved in the third year of medical school (MBChB3) at the University of Glasgow created Virtual Wards. The focus of the Virtual Wards was to continue teaching of clinical reasoning remotely whilst COVID-19 restrictions were in place. Virtual Wards were mapped to the common and important presentations and conditions and provided opportunity for history-taking, clinical examination skills, requesting investigations, interpreting results, diagnosis and management. The Virtual Wards were successful, and further wards were developed the following academic year for MBChB4 students. This chapter describes the theoretical underpinnings of the Virtual Wards and the technological considerations, followed by a description of the Wards themselves. We then analyse an evaluation of the Virtual Wards and provide both a faculty and student perspective. Throughout the chapter, we provide tips for educators developing Virtual Ward environments.

'I wouldn't know what to do with the breasts': the impact of patient gender on medical student confidence and comfort in clinical skills.

BACKGROUND: Previous research has found a relationship between students' gender and attitudes surrounding peer physical examination, but relationship between patient gender and confidence/comfort is less clear. We explored whether patient gender affects medical students' levels of confidence and comfort in clinical examination skills. METHODS: An electronic survey and focus groups were conducted with medical students from one UK institution. Students reported levels of confidence/comfort when carrying out clinical examinations on men/women. An inductive thematic analysis was performed. RESULTS: Of a total of 1500 students provided with the opportunity to participate, ninety (6%) responded. For cardiovascular and respiratory examinations, confidence/comfort were higher when examining male-presenting patients. The opposite was true for mental state examinations. Barriers to confidence/comfort included perceiving males as a norm, difficulty navigating breasts, tutors' internalised gendered attitudes and a wider sociocultural issue. Facilitators of confidence/comfort included students relating to patients, embodying a professional role, gender blindness, and authentic clinical environments. Fewer than 20% (n = 18) of students felt they had enough opportunity to practice clinical skills on women, versus 90% (n = 82) on men. CONCLUSION: Our study identified an area where students' confidence and comfort in clinical examinations could be enhanced within medical education. Changes were implemented in the institution under study's vocational skills teaching, which is rooted in general practice. Information on gender and clinical skills was provided within course handbooks, time was scheduled to discuss gender and clinical skills in small group settings, and equitable gender representation was ensured in clinical assessment.

Collaboration of MYC and RUNX2 in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.

MYC and RUNX oncogenes each trigger p53-mediated failsafe responses when overexpressed in vitro and collaborate with p53 deficiency in vivo. However, together they drive rapid onset lymphoma without mutational loss of p53. This phenomenon was investigated further by transcriptomic analysis of premalignant thymus from RUNX2/MYC transgenic mice. The distinctive contributions of MYC and RUNX to transcriptional control were illustrated by differential enrichment of canonical binding sites and gene ontology analyses. Pathway analysis revealed signatures of MYC, CD3, and CD28 regulation indicative of activation and proliferation, but also strong inhibition of cell death pathways. In silico analysis of discordantly expressed genes revealed Tnfsrf8/CD30, Cish, and Il13 among relevant targets for sustained proliferation and survival. Although TP53 mRNA and protein levels were upregulated, its downstream targets in growth suppression and apoptosis were largely unperturbed. Analysis of genes encoding p53 posttranslational modifiers showed significant upregulation of three genes, Smyd2, Set, and Prmt5. Overexpression of SMYD2 was validated in vivo but the functional analysis was constrained by in vitro loss of p53 in RUNX2/MYC lymphoma cell lines. However, an early role is suggested by the ability of SMYD2 to block senescence-like growth arrest induced by RUNX overexpression in primary fibroblasts.

Student-Created Online Teaching Resources for Students.

Students have long been creating their own visualisations of concepts taught through presentations, posters, figures in essays etc. However, with the introduction of technology, the content created by students is now easily shared with future cohorts of students. This chapter explores the history and advantages of student-created resources for students, then describes the examples of e-tutorials and MOOCs in more detail. Finally, future challenges are identified and discussed.

Insertional mutagenesis and deep profiling reveals gene hierarchies and a Myc/p53-dependent bottleneck in lymphomagenesis.

Retroviral insertional mutagenesis (RIM) is a powerful tool for cancer genomics that was combined in this study with deep sequencing (RIM/DS) to facilitate a comprehensive analysis of lymphoma progression. Transgenic mice expressing two potent collaborating oncogenes in the germ line (CD2-MYC, -Runx2) develop rapid onset tumours that can be accelerated and rendered polyclonal by neonatal Moloney murine leukaemia virus (MoMLV) infection. RIM/DS analysis of 28 polyclonal lymphomas identified 771 common insertion sites (CISs) defining a 'progression network' that encompassed a remarkably large fraction of known MoMLV target genes, with further strong indications of oncogenic selection above the background of MoMLV integration preference. Progression driven by RIM was characterised as a Darwinian process of clonal competition engaging proliferation control networks downstream of cytokine and T-cell receptor signalling. Enhancer mode activation accounted for the most efficiently selected CIS target genes, including Ccr7 as the most prominent of a set of chemokine receptors driving paracrine growth stimulation and lymphoma dissemination. Another large target gene subset including candidate tumour suppressors was disrupted by intragenic insertions. A second RIM/DS screen comparing lymphomas of wild-type and parental transgenics showed that CD2-MYC tumours are virtually dependent on activation of Runx family genes in strong preference to other potent Myc collaborating genes (Gfi1, Notch1). Ikzf1 was identified as a novel collaborating gene for Runx2 and illustrated the interface between integration preference and oncogenic selection. Lymphoma target genes for MoMLV can be classified into (a) a small set of master regulators that confer self-renewal; overcoming p53 and other failsafe pathways and (b) a large group of progression genes that control autonomous proliferation in transformed cells. These findings provide insights into retroviral biology, human cancer genetics and the safety of vector-mediated gene therapy.

Twelve tips for online synchronous small group learning in medical education.

This article was migrated. The article was marked as recommended. Undergraduate medical education relies on a variety of small group learning formats to deliver the curriculum, support collaborative learning, encourage critical thinking, as well as the development of a number of professional, clinical and generic attributes. However, the SARS-CoV-2 (COVID-19) pandemic of 2020 reminded us that unanticipated circumstances may necessitate a rapid and abrupt switch to delivering medical education through alternative means, while still upholding teaching standards and meeting learning and graduate outcomes. For many medical schools, the pandemic resulted in small group teaching being moved to an online format. The experience of students and facilitators moving small group learning tutorials to online synchronous delivery forms the basis for a set of recommendations when considering the delivery of small group teaching remotely.

Runx2 in normal tissues and cancer cells: A developing story.

The Runx transcription factors are essential for mammalian development, most notably in the haematopoietic and osteogenic lineages. Runx1 and its binding partner, CBFbeta, are frequently targeted in acute leukaemia but evidence is accumulating that all three Runx genes may have a role to play in a wider range of cancers, either as tumour promoters or tumour suppressors. Whilst Runx2 is renowned for its role as a master regulator of bone development we discuss here its expression pattern and putative functions beyond this lineage. Furthermore, we review the evidence that RUNX2 promotes neoplastic development in haematopoietic lineages and in advanced mammary and prostate cancer.

Validation of an in vitro single-impact load model of the initiation of osteoarthritis-like changes in articular cartilage.

The objective of this study was the development and characterization of an in vitro model of the initiation of traumatic osteoarthritis (OA). Articular cartilage was obtained from seven healthy horses and from four horses diagnosed with OA. Cartilage disks were subjected to a single-impact load (500 g from 25, 50, or 100 mm) using a simple drop-tower device and cultured in vitro for up to 20 days. Cartilage sections were examined histologically to observe surface damage and proteoglycan loss. Percentage cell death was determined using TUNEL, release of glycosaminoglycans (GAG) to the medium was measured using the DMMB assay, and percentage weight gain calculated. Following a single-impact load and subsequent culture in vitro, articular cartilage explants demonstrated characteristic surface damage, proteoglycan loss, and chondrocyte death. This closely resembled degenerative changes observed in OA cartilage samples. A kinetic study showed that these degenerative changes (increased weight gain, GAG release into the medium, and chondrocyte death) were initiated within 48 h following impact and increased with recovery time in culture. These parameters were proportional to impact height, that is, impact energy. In conclusion, articular cartilage disks subjected to a single-impact load followed by 48 h of recovery time in culture in vitro developed traumatic OA-like changes. These changes can be quantified and compared, making the in vitro single-impact load model a useful tool for the elucidation of the early molecular pathways involved in the process leading from trauma to cartilage degeneration.

Differential signalling mechanisms predisposing primary human skeletal muscle cells to altered proliferation and differentiation: roles of IGF-I and TNFalpha.

To gain a clearer insight into the mechanisms of skeletal muscle cell growth, differentiation and maintenance, we have developed a primary adult human skeletal muscle cell model. Cells were cultured from biopsies of rectus muscle from the anterior abdominal wall of patients undergoing elective surgery. Under differentiating conditions, all cultures formed myotubes, irrespective of initial myoblast number. Stimulation with both IGF-I and tumour necrosis factor alpha (TNFalpha) increased cellular proliferation but while IGF-I subsequently increased myoblast differentiation, via both hyperplasia and hypertrophy, TNFalpha inhibited the initiation of differentiation, but did not induce apoptosis. Addition of IGF-I stimulated both the MAP kinase and the phosphatidylinositide 3-kinase (PI 3-kinase) signalling pathways while treatment with TNFalpha preferentially led to MAP kinase activation although with a very different profile of activation compared to IGF-I. Data using the MEK inhibitor UO126 showed MAP kinase activity is not only needed for cellular proliferation but is also necessary for both the initiation and the progression of primary human myoblast differentiation. The PI 3-kinase pathway is also involved in differentiation, but activation of this pathway could not relieve inhibition of differentiation by TNFalpha or UO126. Our results show that the controlled temporal and amplitude of activation of multiple signalling pathways is needed for successful myoblast differentiation.