Unfolding the empathic insights and tendencies among medical students of two gulf institutions using interpersonal reactivity index.

BACKGROUND: Empathy is an essential core competency for future doctors. Unfortunately, the medical curriculum is infamously known to burn out aspiring doctors, which may potentially lead to a decline in empathy among medical students. This research was planned to understand the evolution of empathic approaches among students across the curriculum using the Interpersonal reactivity index (IRI) as a benchmark at the Royal College of Surgeons in Ireland - Medical University of Bahrain (RCSI-MUB) and University of Sharjah (UoS). METHODS: We adopted a cross-sectional design and administered an online survey to the medical students of RCSI-MUB and UoS using a modified version of the IRI along with its three subscales of empathic concern (EC), perspective taking (PT), and personal distress (PD). To identify intra- and inter-institutional variations in empathy scores, the Analysis of Variance (ANOVA) was performed separately for each institution and with both institutions combined. A two-way ANOVA was conducted for the comparison between years and institutions. For the subscale analysis of EC, PT, and PD, we used one-way ANOVA for significant differences between years at both institutions. For the gender-effect analysis, t-test was performed to examine the differences in total IRI scores at both institutions combined and at each institution separately. Additionally, an Analysis of Covariance (ANCOVA) was done to identify the influence of gender on empathy scores. RESULTS: A total of 140 students from both institutions participated in this study. We found a fluctuating pattern of empathy scores without a clear trend across the years. The sub-scales of EC, PD, and PT across academic years at both institutions showed significant differences within the EC at RCSI-MUB (p = 0.003). No significant differences were identified across other years from both institutions. There were significant differences between empathy scores from RCSI-MUB and UoS for EC (p = 0.011). Additionally, a pronounced interaction effect between year and institution was observed for PT (p = 0.032). The gender-wise analysis showed that female students had higher empathy scores than males (p = 0.004). The ANCOVA for IRI score results revealed a p-value of 0.023, indicating that gender plays a crucial role in empathy levels among medical students. The ANCOVA results revealed a p-value of 0.022 in the EC subscale. CONCLUSION: Our study unveiled intricate patterns in empathy development among medical students across years and genders at RCSI-MUB and UoS. These congruences and dissimilarities in empathy scores signal a subjective understanding of empathy by medical students. The disparities in understanding may encourage medical educators to embed empathy in standard medical curricula for better healthcare outcomes.

HTLV-1 infected T cells cause bone loss via small extracellular vesicles.

Adult T cell leukemia (ATL), caused by infection with human T cell leukemia virus type 1 (HTLV-1), is often complicated by hypercalcemia and osteolytic lesions. Therefore, we studied the communication between patient-derived ATL cells (ATL-PDX) and HTLV-1 immortalized CD4+ T cell lines (HTLV/T) with osteoclasts and their effects on bone mass in mice. Intratibial inoculation of some HTLV/T lead to a profound local decrease in bone mass similar to marrow-replacing ATL-PDX, despite the fact that few HTLV/T cells persisted in the bone. To study the direct effect of HTLV/T and ATL-PDX on osteoclasts, supernatants were added to murine and human osteoclast precursors. ATL-PDX supernatants from hypercalcemic patients promoted formation of mature osteoclasts, while those from HTLV/T were variably stimulatory, but had largely consistent effects between human and murine cultures. Interestingly, this osteoclastic activity did not correlate with expression of osteoclastogenic cytokine RANKL, suggesting an alternative mechanism. HTLV/T and ATL-PDX produce small extracellular vesicles (sEV), known to facilitate HTLV-1 infection. We hypothesized that these sEV also mediate bone loss by targeting osteoclasts. We isolated sEV from both HTLV/T and ATL-PDX, and found they carried most of the activity found in supernatants. In contrast, sEV from uninfected activated T cells had little effect. Analysis of sEV (both active and inactive) by mass spectrometry and electron microscopy confirmed absence of RANKL and intact virus. Viral proteins Tax and Env were only present in sEV from the active, osteoclast-stimulatory group, along with increased representation of proteins involved in osteoclastogenesis and bone resorption. sEV injected over mouse calvaria in the presence of low dose RANKL caused more osteolysis than RANKL alone. Thus, HTLV-1 infection of T cells can cause release of sEV with strong osteolytic potential, providing a mechanism beyond RANKL production that modifies the bone microenvironment, even in the absence of overt leukemia.