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BackgroundMentorship influences career planning, academic productivity, professional satisfaction, and most notably, the pursuit of academic medicine careers. Little is known about the role of mentoring in recruiting Black/African American and Hispanic/Latino residents into academia. The objective of this study was to assess the influence of mentoring on academic medicine career choice among a cohort of racially and ethnically diverse residents.MethodsA strategic convenience sample of U.S. residents attending national professional conferences between March and July 2010; residents completed a quantitative survey and a subset participated in focus groups.ResultsOf the 250 residents, 183 (73%) completed surveys and 48 participated in focus groups. Thirty-eight percent of residents were white, 31% Black/African American, 17% Asian/other, and 14% Hispanic/Latino. Most respondents (93%) reported that mentorship was important for entering academia, and 70% reported having sufficient mentorship to pursue academic careers. Three themes about mentorship emerged from focus groups: (1) qualities of successful mentorship models; (2) perceived benefits of mentorship; and (3) the value of racial/ethnic and gender concordance. Residents preferred mentors they selected rather than ones assigned to them, and expressed concern about faculty using checklists. Black/African American, Hispanic/Latino, and female residents described actively seeking out mentors of the same race/ethnicity and gender, but expressed difficulty finding such mentors. Lack of racial/ethnic concordance was perceived as an obstacle for minority mentees, requiring explanation of the context and nuances of their perspectives and situations to non-minority mentors.ConclusionsThe majority of residents in this study reported having access to mentors. However, data show that the lack of diverse faculty mentors may impede diverse residents’ satisfaction and benefit from mentorship relationships compared to white residents. These findings are important for residency programs striving to enhance resident mentorship and for institutions working to diversify their faculty and staff to achieve institutional excellence.

Numerous studies have reported altered in vitro cytokine production in various diseases. In the present study we used specific immunoassays to quantitate production of interleukin 1 beta (IL 1 beta), IL 1 alpha, tumor necrosis factor (TNF) and IL 2 from human peripheral blood mononuclear cells (PBMC). The distribution of cell-associated and secreted cytokines was studied in PBMC of 21 individuals; in response to lipopolysaccharide (LPS) the proportion of cell-associated IL 1 beta ranged from 13% to 56%, for IL 1 alpha 29% to 98%, and for TNF 2% to 17%. In a larger cohort of 32 subjects, the total amount of immunoreactive cytokines produced in response to LPS or phytohemagglutinin was normally distributed within the study group. Mean production of IL 1 alpha in response to LPS was 10.1 ng/ml and exceeded production of IL 1 beta (5.6 ng/ml) and TNF (2.2 ng/ml). The distribution pattern was characterized by high intersubject variability extending over two orders of magnitude and the presence of high and low "producers". Production of IL 1 alpha and IL 1 beta correlated (R = 0.69). In contrast, production of IL 1 beta did not correlate with production of TNF or IL 2. Indomethacin present during stimulation of PBMC increased the amount of IL 1 beta produced and showed a high correlation (R = 0.83) compared to cultures without indomethacin. Thus, low production of IL 1 beta in certain subjects appears not to be due to inhibitable levels of cyclooxygenase products. In a retrospective study, PBMC from 12 subjects who had taken oral cyclooxygenase inhibitors during the preceding 7 days produced 43% more IL 1 beta than subjects who did not take these drugs (p less than 0.05). These studies demonstrate that the amount of cytokine synthesized by PBMC (a) is regulated independently for IL 1, TNF and IL 2; (b) correlates for IL 1 beta and IL 1 alpha; (c) is intrinsic for low and high "producers", and (d) production of IL 1 beta increases with the use of oral cyclooxygenase inhibitors.