Improving Influenza Vaccination in Hospitalized Children With Asthma.

OBJECTIVES: Children with asthma are at increased risk of complications from influenza; hospitalization represents an important opportunity for vaccination. We aimed to increase the influenza vaccination rate among eligible hospitalized patients with asthma on the pediatric hospital medicine (PHM) service from 13% to 80% over a 4-year period. METHODS: Serial Plan-Do-Study-Act cycles were implemented to improve influenza vaccination rates among children admitted with status asthmaticus and included modifications to the electronic health record (EHR) and provider and family education. Success of the initial PHM pilot led to the development of a hospital-wide vaccination tracking tool and an institutional, nurse-driven vaccine protocol by a multidisciplinary team. Our primary outcome metric was the inpatient influenza vaccination rate among PHM patients admitted with status asthmaticus. Process measures included documentation of influenza vaccination status and use of the EHR asthma order set and a history and physical template. The balance measure was adverse vaccine reaction within 24 hours. Data analysis was performed by using statistical process control charts. RESULTS: The inpatient influenza vaccination rate increased from 13% to 57% over 4 years; special cause variation was achieved. Overall, 50% of eligible patients were vaccinated during asthma hospitalization in the postintervention period. Documentation of influenza vaccination status significantly increased from 51% to 96%, and asthma history and physical and order set use also improved. No adverse vaccine reactions were documented. CONCLUSIONS: A bundle of interventions, including EHR modifications, provider and family education, hospital-wide tracking, and a nurse-driven vaccine protocol, increased influenza vaccination rates among eligible children hospitalized with status asthmaticus.

Publisher Correction: Evidence linking microRNA suppression of essential prosurvival genes with hippocampal cell death after traumatic brain injury.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

Evidence linking microRNA suppression of essential prosurvival genes with hippocampal cell death after traumatic brain injury.

The underlying molecular mechanisms of how dysregulated microRNAs (miRNAs) cause neurodegeneration after traumatic brain injury (TBI) remain elusive. Here we analyzed the biological roles of approximately 600 genes - we previously found these dysregulated in dying and surviving rat hippocampal neurons - that are targeted by ten TBI-altered miRNAs. Bioinformatic analysis suggests that neurodegeneration results from a global miRNA-mediated suppression of genes essential for maintaining proteostasis; many are hub genes - involved in RNA processing, cytoskeletal metabolism, intracellular trafficking, cell cycle progression, repair/maintenance, bioenergetics and cell-cell signaling - whose disrupted expression is linked to human disease. Notably, dysregulation of these essential genes would significantly impair synaptic function and functional brain connectivity. In surviving neurons, upregulated miRNA target genes are co-regulated members of prosurvival pathways associated with cellular regeneration, neural plasticity, and development. This study captures the diversity of miRNA-regulated genes that may be essential for cell repair and survival responses after TBI.