Bridging the gap: increasing collaboration between research mentors and career development educators for PhD and postdoctoral training success

National reports and funding mandates have called for trainee-centered PhD and postdoctoral training and the need to support diverse career outcomes. As a result, career and professional development (CPD) resources have expanded at several institutions. Despite the growth of innovative and impactful CPD resources, access to and awareness of resources have been inconsistent and inequitable for graduate and postdoctoral trainees. In the current model, core education occurs in two unconnected ways: faculty research mentors provide scientific competencies training, while CPD educators provide transferable competencies training, which is separate from the curriculum and optional at most institutions. Research mentors are influential in supporting trainee engagement with CPD programs; however, most are either unaware of the rapidly growing opportunities or may not see the direct benefit to scientific development and productivity. Due to this disconnect, some trainees can be inadvertently distanced from CPD resources, leading to more inequities among groups. To bridge this gap, here we propose a realignment of the current model via a set of practical and collaborative solutions providing benefit to all stakeholders. With greater awareness and collaboration, research mentors and CPD educators can complement each other’s expertise to better support trainee experiences and outcomes

Non-disjunction of chromosome 13

We performed a molecular study with 21 microsatellites on a sample of 82 trisomy 13 conceptuses, the largest number of cases studied to date. The parental origin was determined in every case and in 89% the extra chromosome 13 was of maternal origin with an almost equal number of maternal MI and MII errors. The latter finding is unique among human autosomal trisomies, where maternal MI (trisomies 15, 16, 21, 22) or MII (trisomy 18) errors dominate. Of the nine paternally derived cases five were of MII origin but none arose from MI errors. There was some evidence for elevated maternal age in cases with maternal meiotic origin for liveborn infants. Maternal and paternal ages were elevated in cases with paternal meiotic origin. This is in contrast to results from a similar study of non-disjunction of trisomy 21 where paternal but not maternal age was elevated. We find clear evidence for reduced recombination in both maternal MI and MII errors and the former is associated with a significant number of tetrads (33%) that are nullichiasmate, which do not appear to be a feature of normal chromosome 13 meiosis. This study supports the evidence for subtle chromosome-specific influences on the mechanisms that determine non-disjunction of human chromosomes, consistent with the diversity of findings for other trisomie