Piloting Medication Histories in a Pediatric Postanesthesia Care Unit.

PURPOSE: Develop a medication history process for pediatric postanesthesia care unit (PACU) patients to identify discrepancies between home and inpatient medications and prevent medication errors. DESIGN: Pilot an evidence-based practice change to perform PACU medication histories. METHODS: Inpatients or surgical admissions to general care units at a pediatric tertiary care 348-bed hospital ages 2-18 years were included. Parents/guardians were asked about their child's prescription and over-the-counter medications, allergies, and adherence. Data included patient age, surgery, medication categories, and error classifications. Information was compared to the patient's medical record. FINDINGS: From June to July 2016, 75 medication histories were performed, covering 44.6% of eligible cases within the period. Seventy-four discrepancies were found, the most frequent being omission. The medication category with the most errors was vitamins/herbals/supplements. CONCLUSION: The workflow designed assessed discrepancy frequency and type in surgical patients' medication lists when transitioning from the PACU to general care units.

C/EBPα is an essential collaborator in Hoxa9/Meis1-mediated leukemogenesis.

Homeobox A9 (HOXA9) is a homeodomain-containing transcription factor that plays a key role in hematopoietic stem cell expansion and is commonly deregulated in human acute leukemias. A variety of upstream genetic alterations in acute myeloid leukemia (AML) lead to overexpression of HOXA9, almost always in association with overexpression of its cofactor meis homeobox 1 (MEIS1) . A wide range of data suggests that HOXA9 and MEIS1 play a synergistic causative role in AML, although the molecular mechanisms leading to transformation by HOXA9 and MEIS1 remain elusive. In this study, we identify CCAAT/enhancer binding protein alpha (C/EBPα) as a critical collaborator required for Hoxa9/Meis1-mediated leukemogenesis. We show that C/EBPα is required for the proliferation of Hoxa9/Meis1-transformed cells in culture and that loss of C/EBPα greatly improves survival in both primary and secondary murine models of Hoxa9/Meis1-induced leukemia. Over 50% of Hoxa9 genome-wide binding sites are cobound by C/EBPα, which coregulates a number of downstream target genes involved in the regulation of cell proliferation and differentiation. Finally, we show that Hoxa9 represses the locus of the cyclin-dependent kinase inhibitors Cdkn2a/b in concert with C/EBPα to overcome a block in G1 cell cycle progression. Together, our results suggest a previously unidentified role for C/EBPα in maintaining the proliferation required for Hoxa9/Meis1-mediated leukemogenesis.