RESUMEN
OBJECTIVES: Within the past several years, innovative communication tools have been established as viable quality improvement mechanisms in health care. Meanwhile, the economic and societal burdens of hospital-acquired conditions (HACs) continue to rise. Various interventions have been attempted to reduce HACs. This study evaluated the effectiveness of a communication tool in reducing risk factors for HACs. METHODS: A communication tool aimed at reducing HAC risk factors was developed by an interdisciplinary team of physicians and nurses and tested in a simple before-after quality improvement study. It included 8 components: ambulation/fall risk, blood glucose greater than 200 mg/dL, central venous catheters, deep venous thrombosis prophylaxis, erosions of the skin/dermal ulcers, Foley/urinary catheters, got communication, and heart monitor/telemetry. This communication tool facilitated multidisciplinary communication. The nurses completed it nightly, and the physicians reviewed the communication tool each morning and, when appropriate, addressed components of care that were out of compliance with best practices. RESULTS: The use of the ABCs of Hospitalized Patients Communication Tool led to daily improvements with reduction in the percentage of patients with blood glucose greater than 200 mg/dL from 43.3% to 35.1%, reduction in the use of central venous catheters from 8.2% to 1.0% of patients, increase in the use of chemical deep venous thrombosis prophylaxis from 45.4% of patients to 56.7%, reduction in the use of urinary catheters from 27.6% to 13.2%, and decrease in use of telemetry from 67.5% to 55.1%. All of the results have P < 0.05. These improvements were sustained over time. CONCLUSIONS: Implementation of a multidisciplinary communication tool serves as a simple, resource-conscious, and customizable instrument to reduce the risk factors for developing HACs. This communication tool can be easily disseminated and used by other institutions.
Asunto(s)
Estudios Controlados Antes y Después/métodos , Hospitalización/tendencias , Mejoramiento de la Calidad/normas , Adulto , Comunicación , Femenino , Humanos , MasculinoRESUMEN
Certain chromosome rearrangements, found in cancer cells or in cells exposed to ionizing radiation, exhibit a chromosome-wide delay in replication timing (DRT) that is associated with a delay in mitotic chromosome condensation (DMC). We have developed a chromosome engineering strategy that allows the generation of chromosomes with this DRT/DMC phenotype. We found that approximately 10% of inter-chromosomal translocations induced by two distinct mechanisms, site-specific recombination mediated by Cre or non-homologous end joining of DNA double-strand breaks induced by I-Sce1, result in DRT/DMC. Furthermore, on certain balanced translocations only one of the derivative chromosomes displays the phenotype. Finally, we show that the engineered DRT/DMC chromosomes acquire gross chromosomal rearrangements at an increased rate when compared with non-DRT/DMC chromosomes. These results indicate that the DRT/DMC phenotype is not the result of a stochastic process that could occur at any translocation breakpoint or as an epigenetic response to chromosome damage. Instead, our data indicate that the replication timing of certain derivative chromosomes is regulated by a cis-acting mechanism that delays both initiation and completion of DNA synthesis along the entire length of the chromosome. Because chromosomes with DRT/DMC are common in tumor cells and in cells exposed to ionizing radiation, we propose that DRT/DMC represents a common mechanism responsible for the genomic instability found in cancer cells and for the persistent chromosomal instability associated with cells exposed to ionizing radiation.
Asunto(s)
Momento de Replicación del ADN/genética , Replicación del ADN , Inestabilidad Genómica/genética , Neoplasias/genética , Translocación Genética , Línea Celular Tumoral , Deleción Cromosómica , Ingeniería Genética/métodos , HumanosRESUMEN
Certain chromosome rearrangements display a significant delay in replication timing that is associated with a delay in mitotic chromosome condensation. Chromosomes with delay in replication timing/delay in mitotic chromosome condensation participate in frequent secondary rearrangements, indicating that cells with delay in replication timing/delay in mitotic chromosome condensation display chromosomal instability. In this report, we show that exposing cell lines or primary blood lymphocytes to ionizing radiation results in chromosomes with the delay in replication timing/delay in mitotic chromosome condensation phenotype, and that the delay in replication timing/delay in mitotic chromosome condensation phenotype occurs predominantly on chromosome translocations. In addition, exposing mice to ionizing radiation also induces cells with delay in replication timing/delay in mitotic chromosome condensation chromosomes that persist for as long as 2 years. Cells containing delay in replication timing/delay in mitotic chromosome condensation chromosomes frequently display hyperdiploid karyotypes, indicating that delay in replication timing/delay in mitotic chromosome condensation is associated with aneuploidy. Finally, using a chromosome engineering strategy, we show that only a subset of chromosome translocations displays delay in replication timing/delay in mitotic chromosome condensation. Our results indicate that specific chromosome rearrangements result in the generation of the delay in replication timing/delay in mitotic chromosome condensation phenotype and that this phenotype occurs frequently in cells exposed to ionizing radiation both in vitro and in vivo.