Providing context for a medical school basic science curriculum: The importance of the humanities

Introduction: To increase students’ understanding of what it means to be a physician and engage in the everyday practice of medicine, a humanities program was implemented into the preclinical curriculum of the medical school curriculum. The purpose of our study was to determine how medical students’ views of being a doctor evolved after participating in a required humanities course.

Methods: Medical students completing a 16-clock hour humanities course from 10 courses were asked to respond to an open-ended reflection question regarding changes, if any, of their views of being a doctor. The constant comparative method was used for coding; triangulation and a variety of techniques were used to provide evidence of validity of the analysis.

Results: A majority of first- and second-year medical students (rr?=?70%) replied, resulting in 100 pages of text. A meta-theme of Contextualizing the Purpose of Medicine and three subthemes: the importance of Treating Patients Rather than a Disease, Understanding Observation Skills are Important, and Recognizing that Doctors are Fallible emerged from the data.

Conclusions: Results suggest that requiring humanities as part of the required preclinical curriculum can have a positive influence on medical students and act as a bridge to contextualize the purpose of medicine.     

Nidogen 1 regulates proliferation and migration/invasion in murine claudin-low mammary tumor cells

Nidogen 1 (NID1) is a glycoprotein found in basement membranes involved in cross-linking collagen IV and laminin. The role of NID in breast cancer has only been evaluated in a small number of studies and the findings of these studies have been inconsistent. Our previous work revealed that highly tumorigenic murine mammary tumor cells express high levels of Nid1 while weakly tumorigenic mammary tumor cells express low levels of Nid1. To investigate Nid1, two stable knockdown lines were created, and Nid1 knockdown was confirmed at both the mRNA and protein level. Nid1 knockdown significantly reduced cell proliferation and migration/invasion and these reductions in proliferation and migration/invasion could be rescued by conditioned media containing NID1 protein. The reduced migration/invasion observed in the Nid1 knockdown cells was not associated with significant alterations in the epithelial gene Cdh1 or the mesenchymal genes Snai1, Snai2, Twist1, Twist2, Zeb1 and Zeb2. Therefore, suppression of Nid1 expression reduces proliferation and migration/invasion in claudin-low murine mammary tumor cells.