Objectives The coronavirus disease 2019 (COVID‐19) pandemic has led to widespread disruptions in the clinical education of medical students. In managing students’ return to the clinical setting, medical schools face the challenge of balancing education, service and risk considerations. To compound this challenge, medical students may prefer not to re‐enter during a period of great uncertainty, leading to substantive downstream sequelae on individual, institutional and national levels. Understanding students’ views on resuming clinical experiences, therefore, is an important consideration. The purpose of this study was to assess medical students’ preference for re‐entering the clinical setting during the COVID‐19 pandemic and to explore personal and environmental characteristics associated with that preference. Methods We conducted an electronic survey of currently enrolled medical students at the Duke‐NUS Medical School, less than a month into the COVID‐19 pandemic. Survey items were aligned with a conceptual framework related to medical students’ preference for returning to the clinical setting. The framework consisted of three domains: (a) non‐modifiable demographic information; (b) factors thought to be modifiable through the course of medical education, including burnout, tolerance for ambiguity, motivation and professionalism, and (c) students’ perception of COVID‐19 infection risk to self. Results Approximately one‐third (n=63) of 179 students preferred not to return to the clinical setting. Results of a multivariable analysis indicated that compared to this group, the two‐thirds (n=116) of students favouring return showed evidence of greater autonomous (or internal) motivation, a greater sense of professional responsibility and a lower self‐perception of harbouring risk to patients. Conclusions Students’ preference on returning to the clinical environment stems from the interplay of several key factors, and is substantively associated with perceptions of professional responsibility and their own potential risk to the health care system. Mindfully considering and addressing these issues may help medical schools in their preparation for returning students to the clinical setting.
Background Professional identity formation (PIF) in medical students is a multifactorial phenomenon, shaped by ways that clinical and non-clinical experiences, expectations and environmental factors merge with individual values, beliefs and obligations. The relationship between students’ evolving professional identity and self-identity or personhood remains ill-defined, making it challenging for medical schools to support PIF systematically and strategically. Primarily, to capture prevailing literature on PIF in medical school education, and secondarily, to ascertain how PIF influences on medical students may be viewed through the lens of the ring theory of personhood (RToP) and to identify ways that medical schools support PIF. Methods A systematic scoping review was conducted using the systematic evidence-based approach. Articles published between 1 January 2000 and 1 July 2020 related to PIF in medical students were searched using PubMed, Embase, PsycINFO, ERIC and Scopus. Articles of all study designs (quantitative and qualitative), published or translated into English, were included. Concurrent thematic and directed content analyses were used to evaluate the data. Results A total of 10443 abstracts were identified, 272 full-text articles evaluated, and 76 articles included. Thematic and directed content analyses revealed similar themes and categories as follows: characteristics of PIF in relation to professionalism, role of socialization in PIF, PIF enablers and barriers, and medical school approaches to supporting PIF. Discussion PIF involves iterative construction, deconstruction and inculcation of professional beliefs, values and behaviours into a pre-existent identity. Through the lens of RToP, factors were elucidated that promote or hinder students’ identity development on individual, relational or societal levels. If inadequately or inappropriately supported, enabling factors become barriers to PIF. Medical schools employ an all-encompassing approach to support PIF, illuminating the need for distinct and deliberate longitudinal monitoring and mentoring to foster students’ balanced integration of personal and professional identities over time.
Hepatic metastasis is a primary cause for failure of locoregional therapy in colorectal cancer. Increased expression of osteopontin (OPN), a ligand for alpha(v)beta3 integrin and CD44 receptors, is associated with metastasis in several types of cancer. However, the mechanism by which OPN mediates metastasis in colorectal cancer remains unknown. We hypothesized that OPN mediates invasion of colon cancer cells through basement membrane and migration through extracellular matrix (ECM). In this study, we used CT26 murine colon adenocarcinoma cells syngeneic to BALB/c mice to generate cell lines (pS-OPN) in which OPN expression was suppressed through small interfering RNA (siRNA) plasmids. CT26 wild-type cells (WT) and CT26 cells stably expressing murine-mismatch siRNA (pS-MM) served as controls. Western blotting quantified OPN protein levels and our most downregulated clone, pS-OPN-A4, demonstrated a mean 3.0-fold decrease in OPN protein expression versus WT. In vitro cell motility and invasiveness were decreased in pS-OPN-A4 by 3.6-fold (P = 0.004 versus WT) and 4.1-fold (P = 0.01 versus WT), but proliferation was similar amongst cell lines. We demonstrated that OPN suppression significantly correlates with MMP-2 downregulation. In vivo hepatic metastasis was assessed by quantifying liver weights and surface tumor nodules in 33 BALB/c mice (11/group) subjected to intrasplenic injection of tumor cells. pS-OPN-A4 resulted in a 50.4% decrease in mean liver weight compared with WT (3.79 +/- 1.49 g versus 1.88 +/- 1.34 g, P = 0.009). Only 18% of pS-OPN-A4 livers had >20 metastatic surface nodules compared with 89% for WT and 75% for pS-MM-V6. This study demonstrates that RNA interference stably reduces CT26 tumor expression of OPN and significantly attenuates CT26 colon cancer metastasis by diminishing tumor cell motility and invasiveness.
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