Empathy in Medical Education:Its Nature and Nurture — a Qualitative Study of the Views of Students and Tutors

CONTEXT: Medical education is committed to teaching patient centred communication and empathy. However, quantitative research suggests empathy scores tend to decline as students progress through medical school. In qualitative terms, there is a need to better understand how students and tutors view the practice and teaching of clinical empathy and the phenomenon of empathic erosion. METHODS: Working within a constructivist paradigm, researchers thematically analysed the individual interview data from a purposive sample of 13 senior students and 9 tutors. RESULTS: The four major themes were as follows: (1) ‘the nature of empathy’, including the concept of the innate empathy that students already possess at the beginning of medical school; (2) ‘beyond the formal curriculum’ and the central importance of role modelling; (3) ‘the formal curriculum and the tick-box influence of assessments’; and (4) the ‘durability of empathy’, including ethical erosion and resilience. A garden model of empathy development is proposed — beginning with the innate seeds of empathy that students bring to medical school, the flowering of empathy is a fragile process, subject to both enablers and barriers in the formal, informal, and hidden curricula. CONCLUSION: This study provides insights into empathic erosion in medical school, including the problems of negative role modelling and the limitations of an assessment system that rewards ‘tick-box’ representations of empathy, rather than true acts of compassion. It also identifies factors that should enable the flowering of empathy, such as new pedagogical approaches to resilience and a role for the arts and humanities

Ibuprofen, Flurbiprofen, Etoricoxib or Paracetamol Do Not Influence ACE2 Expression and Activity In Vitro or in Mice and Do Not Exacerbate In-Vitro SARS-CoV-2 Infection

SARS-CoV-2 uses the human cell surface protein angiotensin converting enzyme 2 (ACE2) as the receptor by which it gains access into lung and other tissue. Early in the pandemic, there was speculation that a number of commonly used medications—including ibuprofen and other non-steroidal anti-inflammatory drugs (NSAIDs)—have the potential to upregulate ACE2, thereby possibly facilitating viral entry and increasing the severity of COVID-19. We investigated the influence of the NSAIDS with a range of cyclooxygenase (COX)1 and COX2 selectivity (ibuprofen, flurbiprofen, etoricoxib) and paracetamol on the level of ACE2 mRNA/protein expression and activity as well as their influence on SARS-CoV-2 infection levels in a Caco-2 cell model. We also analysed the ACE2 mRNA/protein levels and activity in lung, heart and aorta in ibuprofen treated mice. The drugs had no effect on ACE2 mRNA/protein expression and activity in the Caco-2 cell model. There was no up-regulation of ACE2 mRNA/protein expression and activity in lung, heart and aorta tissue in ibuprofen-treated mice in comparison to untreated mice. Viral load was significantly reduced by both flurbiprofen and ibuprofen at high concentrations. Ibuprofen, flurbiprofen, etoricoxib and paracetamol demonstrated no effects on ACE2 expression or activity in vitro or in vivo. Higher concentrations of ibuprofen and flurbiprofen reduced SARS-CoV-2 replication in vitro