Addicts and Admits: Metonymy in Medical Students' Reflective Writing.

Phenomenon: Metonymy refers to the substitution of the name of an attribute or adjunct for the name of the object or person being described. In medical contexts, this may involve referring to a person as a disease, body part, or other health-related noun. In this study, we explore the use of metonymy in medical students' reflective writing. Approach: Using content analysis, we identified all usages of metonymy in a sample of 802 medical student reflective essays. We analyzed them for associated themes and used the Fisher's exact test to compare frequencies of clinical ethics themes that occurred in the essays with metonymy to those without metonymy. Findings: Metonymy was used 60 times in the essays. The uses were grouped into thematic clusters of substance abuse (n = 27), illness (n = 9), body part (n = 4), clinical status (n = 6), reproductive health (n = 5), challenging clinical situations (n = 6), and other thoughts on patients as people (n = 3). Several ethical themes associated with essays using metonymy (p < .05): moral distress, substance abuse, adequate treatment, jumping to conclusions, awakening, and pain. Insights: Metonymy was relatively uncommon, and some students explicitly described the practice as dehumanizing to patients. Even so, metonymy did present in a variety of forms and was used most frequently to describe individuals with substance use disorders. Essays involving metonymy were more likely to describe a scenario that elicited moral distress in the students, which may indicate that metonymy occurs more frequently in some troubling situations.

Reciprocal responsiveness to interleukin-12 and interferon-alpha specifies human CD8+ effector versus central memory T-cell fates.

Multiple innate signals regulate the genesis of effector and memory CD8+ T cells. In this study, we demonstrate that the innate cytokines interleukin (IL)-12 and interferon (IFN)-alpha/beta regulate distinct aspects of effector and memory human CD8+ T-cell differentiation. IL-12 exclusively promoted the development of IFN-gamma- and tumor necrosis factor (TNF)-alpha-secreting T effector memory (T(EM)) cells, whereas IFN-alpha drove the development of T central memory (T(CM)) cells. The development of T(EM) and T(CM) was linked to cell division. In rapidly dividing cells, IL-12 programmed T(EM) through induction of the IL-12 receptor beta2. In contrast, IFN-alpha regulated T(CM) development by slowing the progression of cell division in a subpopulation of cells that selectively expressed elevated IFN-alpha/beta receptor-2. The strength of signal delivered through T-cell receptor (TCR) engagement regulated the responsiveness of cells to IL-12 and IFN-alpha. In the presence of both IL-12 and IFN-alpha, these cytokine signals were amplified as the strength of the TCR signal was increased, promoting the simultaneous development of both T(CM) and T(EM). Together, our results support a novel model in which IL-12 and IFN-alpha act in a nonredundant manner to regulate the colinear generation of both effector and memory cells.