Publications

Approximately one-third of the US population lives at or near the poverty line; however, this group makes up less than 7% of the incoming medical students. In the United Kingdom, the ratio of those of the highest social stratum is 30 times greater than those of the lowest to receive admission to medical school. In an effort to address health disparities and improve patient care, the authors argue that significant barriers must be overcome for the children of the disadvantaged to gain admission to medical school. Poverty is intergenerational and multidimensional. Familial wealth affects opportunities and educational attainment, starting when children are young and compounding as they get older. In addition, structural and other barriers exist to these students pursuing higher education, such as the realities of financial aid and the shadow of debt. Yet the medical education community can take steps to better support the children of the disadvantaged throughout their education, so they are able to reach medical school. If educators value the viewpoints and life experiences of diverse students enriching the learning environment, they must acknowledge the unique contributions that the children of the disadvantaged bring and work to increase their representation in medical schools and the physician workforce. We describe who the disadvantaged are contrasted with the metrics used by medical school admissions to identify them. The consequences of multiple facets of poverty on educational attainment are explored, including its interaction with other social identities, inter-generational impacts, and the importance of wealth versus annual income. Structural barriers to admission are reviewed. Given the multi-dimensional and cumulative nature of poverty, we conclude that absent significant and sustained intervention, medical school applicants from disadvantaged backgrounds will remain few and workforce issues affecting the care patients receive will not be resolved. The role of physicians and medical schools and advocating for necessary societal changes to alleviate this dynamic are highlighted.

Alveolar type I (TI) cells are large squamous cells that cover >95% of the internal surface area of the lung; type II (TII) cells are small cuboidal cells with distinctive intracellular surfactant storage organelles. Based on autoradiographic studies in the 1970s, the long-held paradigm of alveolar epithelial development has been a linear progression from undifferentiated progenitor cells through TII cells to TI cells. Subsequent data support the existence of more complex pathways. Recently, a bipotent TI/TII progenitor cell at embryonic day E18 has been inferred both from marker expression in developing airways and from statistical analyses of gene expression data obtained from single-lung embryonic cells. To study cell lineage directly by fate mapping, we developed new transgenic mouse models in which rtTA is driven either by the rat podoplanin or the mouse Sftpc gene to mark cells irreversibly in development. Using these models, we found two distinct lineage pathways. One pathway, evident as early as E12-15, is devoted almost exclusively to TI cell development; a second pathway gives rise predominantly to TII cells but also a subpopulation of TI cells. We have defined the molecular phenotypes of these distinct progenitor populations and have identified potential regulatory factors in TI and TII cell differentiation. By analyzing gene pathways in mature TI and TII cells, we identified potential novel functions of each cell type. These results provide novel insights into lung development and suggest a basis for testing strategies to promote alveolar differentiation and repair, including potential transplantation of lineage-specific progenitor cells.