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1.
Neurol Clin Pract ; 14(2): e200270, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38524835

RESUMEN

Background and Objectives: Medication reconciliation errors are a common problem in health care, particularly during transitions of care. Discharge medication reconciliation (DMR) errors in a pediatric setting can range from 26% to 42.2%. We conducted a quality improvement project to decrease DMR error rate at Dayton Children's Hospital in Dayton, Ohio. Methods: We conducted 2 interventions, each with 3 Plan-Do-Study-Act cycles from September 2021 through February 2023. The first intervention focused on using current specialty neurology nurses as scribes and creating a template note to include the plan of care and review of DMR before discharge. Our second intervention consisted of standardizing the seizure rescue medication order by creating an order panel within our electronic medical record system for all the rescue medications presently available. Medication errors were documented by the specialty neurology nurse during a phone conversation on the next business day post discharge. DMR error rates were calculated for each week using a control chart. Medication errors and patient harm were classified according to the National Coordinating Council for Medication Error Reporting and Prevention Index. Results: One hundred six errors were noted. Of these, 98 (92%) occurred in patients with seizure and 64 (60%) were related to prescription of seizure rescue medication specifically. The baseline error rate was calculated at 15.7% or 7 errors per month (January 2021 through June 2021). The average error rate dropped from 15.7% to 5.3% (2 errors per month) after initiation of our first intervention (September 2021). Twelve weeks after initiation of the second intervention, a 2.9% (1 error per month) was noted. Afterward, there was a ten-week period of 0% errors. Discussion: Sustainable reduction of DMR errors in pediatric patients with epilepsy was achieved by using specialty neurology nurses to scribe the care plan and creating order panels to facilitate accuracy of discharge medication orders without additional cost to the hospital.

2.
Arch Dermatol Res ; 305(8): 733-9, 2013 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-23589096

RESUMEN

ΔNp63α maintains the proliferative potential of keratinocytes by inhibiting the transcription and nuclear localization of the tumor suppressor PTEN as shown earlier by our laboratory. The goal of this study was to define the mechanisms by which ΔNp63α mediates the nuclear exclusion of PTEN. We demonstrate here that ΔNp63α reduces the ubiquitination of PTEN, a key signaling event in the nuclear translocation of PTEN. The decrease in ubiquitinated PTEN correlated with the ability of ΔNp63α to bind to neuronal precursor developmentally down regulated 4 (NEDD4) promoter and transcriptionally repress the E3 ubiquitin ligase NEDD4-1. Knockdown of NEDD4-1 in cultured keratinocytes was sufficient to attenuate the increase in nuclear PTEN observed upon silencing of ΔNp63α. In vivo examination of normal skin demonstrated that ΔNp63α and NEDD4-1 were both expressed in the basal layer of the epidermis and this correlated with nuclear exclusion of PTEN. Altogether, these studies suggest that ΔNp63α-mediated suppression of nuclear PTEN in basal layer keratinocytes occurs through repression of NEDD4-1.


Asunto(s)
Transporte Activo de Núcleo Celular , Complejos de Clasificación Endosomal Requeridos para el Transporte/metabolismo , Queratinocitos/metabolismo , Fosfohidrolasa PTEN/metabolismo , Factores de Transcripción/metabolismo , Proteínas Supresoras de Tumor/metabolismo , Ubiquitina-Proteína Ligasas/metabolismo , Línea Celular , Proliferación Celular , Regulación hacia Abajo , Complejos de Clasificación Endosomal Requeridos para el Transporte/antagonistas & inhibidores , Complejos de Clasificación Endosomal Requeridos para el Transporte/genética , Epidermis/metabolismo , Humanos , Ubiquitina-Proteína Ligasas Nedd4 , Regiones Promotoras Genéticas , Transducción de Señal , Factores de Transcripción/genética , Proteínas Supresoras de Tumor/genética , Ubiquitina-Proteína Ligasas/antagonistas & inhibidores , Ubiquitina-Proteína Ligasas/genética , Ubiquitinación
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