TRainee Attributable & Automatable Care Evaluations in Real-time (TRACERs): A Scalable Approach for Linking Education to Patient Care.

Competency-based medical education (CBME) is an outcomes-based approach to education and assessment that focuses on what competencies trainees need to learn in order to provide effective patient care. Despite this goal of providing quality patient care, trainees rarely receive measures of their clinical performance. This is problematic because defining a trainee's learning progression requires measuring their clinical performance. Traditional clinical performance measures (CPMs) are often met with skepticism from trainees given their poor individual-level attribution. Resident-sensitive quality measures (RSQMs) are attributable to individuals, but lack the expeditiousness needed to deliver timely feedback and can be difficult to automate at scale across programs. In this eye opener, the authors present a conceptual framework for a new type of measure - TRainee Attributable & Automatable Care Evaluations in Real-time (TRACERs) - attuned to both automation and trainee attribution as the next evolutionary step in linking education to patient care. TRACERs have five defining characteristics: meaningful (for patient care and trainees), attributable (sufficiently to the trainee of interest), automatable (minimal human input once fully implemented), scalable (across electronic health records [EHRs] and training environments), and real-time (amenable to formative educational feedback loops). Ideally, TRACERs optimize all five characteristics to the greatest degree possible. TRACERs are uniquely focused on measures of clinical performance that are captured in the EHR, whether routinely collected or generated using sophisticated analytics, and are intended to complement (not replace) other sources of assessment data. TRACERs have the potential to contribute to a national system of high-density, trainee-attributable, patient-centered outcome measures.

JLP-centrosome is essential for the microtubule-mediated nucleocytoplasmic transport induced by extracellular stimuli.

JLP belongs to the JIP family whose members serve as scaffolding proteins that link motor proteins and their cargo for intracellular transport. Although JLP is mainly cytoplasmic, it accumulates as a focus in the perinuclear region when stimulated by extracellular stimuli. Focus formation, which changes the nucleus shape and concentrates the nuclear pores, depends on p38MAPK activation and the dynein retrograde motor protein complex. Extracellular stimuli trigger the tethering of PLK1 to the centrosome by JLP, leading to centrosome maturation and microtubule array formation. The centrosome localization domain of JLP is important for the binding of the centrosome and the formation of the JLP focus and the microtubule array. Furthermore, the formation of the JLP focus and the microtubule array is interdependent and important for the transport of NF-κB p65 to the nucleus and its unloading therein. In conclusion, JLP exhibits multiple functions in the nuclear translocation of NF-κB p65.

HOP-1 Presenilin Deficiency Causes a Late-Onset Notch Signaling Phenotype That Affects Adult Germline Function in Caenorhabditis elegans.

Functionally redundant genes present a puzzle as to their evolutionary preservation, and offer an interesting opportunity for molecular specialization. In Caenorhabditis elegans, either one of two presenilin genes (sel-12 or hop-1) facilitate Notch activation, providing the catalytic subunit for the γ secretase proteolytic enzyme complex. For all known Notch signaling events, sel-12 can mediate Notch activation, so the conservation of hop-1 remains a mystery. Here, we uncover a novel "late-onset" germline Notch phenotype in which HOP-1-deficient worms fail to maintain proliferating germline stem cells during adulthood. Either SEL-12 or HOP-1 presenilin can impart sufficient Notch signaling for the establishment and expansion of the germline, but maintenance of an adult stem cell pool relies exclusively on HOP-1-mediated Notch signaling. We also show that HOP-1 is necessary for maximum fecundity and reproductive span. The low-fecundity phenotype of hop-1 mutants can be phenocopied by switching off glp-1/Notch function during the last stage of larval development. We propose that at the end of larval development, dual presenilin usage switches exclusively to HOP-1, perhaps offering opportunities for differential regulation of the germline during adulthood. Additional defects in oocyte size and production rate in hop-1 and glp-1 mutants indicate that the process of oogenesis is compromised when germline Notch signaling is switched off. We calculate that in wild-type adults, as much as 86% of cells derived from the stem cell pool function to support oogenesis. This work suggests that an important role for Notch signaling in the adult germline is to furnish a large and continuous supply of nurse cells to support the efficiency of oogenesis.