Quantifying paediatric intensive care unit staffing levels at a paediatric academic medical centre: A mixed-methods approach.

AIM: To identify, simulate and evaluate the formal and informal patient-level and unit-level factors that nurse managers use to determine the number of nurses for each shift. BACKGROUND: Nurse staffing schedules are commonly set based on metrics such as midnight census that do not account for seasonality or midday turnover, resulting in last-minute adjustments or inappropriate staffing levels. METHODS: Staffing schedules at a paediatric intensive care unit (PICU) were simulated based on nurse-to-patient assignment rules from interviews with nursing management. Multivariate regression modelled the discrepancies between scheduled and historical staffing levels and constructed rules to reduce these discrepancies. The primary outcome was the median difference between simulated and historical staffing levels. RESULTS: Nurse-to-patient ratios underestimated staffing by a median of 1.5 nurses per shift. Multivariate regression identified patient turnover as the primary factor accounting for this difference and subgroup analysis revealed that patient age and weight were also important. New rules reduced the difference to a median of 0.07 nurses per shift. CONCLUSION: Measurable, predictable indicators of patient acuity and historical trends may allow for schedules that better match demand. IMPLICATIONS FOR NURSING MANAGEMENT: Data-driven methods can quantify what drives unit demand and generate nurse schedules that require fewer last-minute adjustments.

SNHG7 is a lncRNA oncogene controlled by Insulin-like Growth Factor signaling through a negative feedback loop to tightly regulate proliferation.

Evidence suggests Insulin-like growth factor 1 (IGF1) signaling is involved in the initiation and progression of a subset of breast cancers by inducing cell proliferation and survival. Although the signaling cascade following IGF1 receptor activation is well-studied, the key elements of the transcriptional response governing IGF1's actions are not well understood. Recent studies reveal that the majority of the genome is transcribed and that there are more long non-coding RNAs (lncRNAs) than protein coding genes, several of which are dysregulated in human cancer. However, studies on the regulation and mechanism of action of these lncRNAs are in their infancy. Here we show that IGF1 alters the expression levels of a subset of lncRNAs. SNHG7, a member of the small nucleolar host gene family, is a highly-expressed lncRNA that is consistently and significantly down-regulated by IGF1 signaling by a post-transcriptional mechanism through the MAPK pathway. SNHG7 regulates proliferation of breast cancer cell lines in a dose-dependent manner, and silencing SNHG7 expression causes cell cycle arrest in G0/G1. Intriguingly, SNHG7 alters the expression of many IGF1 signaling intermediates and IGF1-regulated genes suggesting a feedback mechanism to tightly regulate the IGF1 response. Finally, we show in clinical data that SNHG7 is overexpressed in tumors of a subset of breast cancer patients and that these patients have lower disease-free survival than patients without elevated SNHG7 expression. We propose that SNHG7 is a lncRNA oncogene that is controlled by growth factor signaling in a feedback mechanism to prevent hyperproliferation, and that this regulation can be lost in the development or progression of breast cancer.