Patient communication during handovers between emergency medicine and internal medicine residents.

BACKGROUND: Communication failures are a key cause of medical errors and are particularly prevalent during handovers of patients between services. OBJECTIVE: To explore current perceptions of effectiveness in communicating critical patient information during admission handovers between emergency medicine (EM) residents and internal medicine (IM) residents. METHODS: Study design was a survey of IM and EM residents at a large urban hospital. Residents were surveyed about whether critical information was communicated during patient handovers. Measurements included comparisons between IM and EM residents about their perceptions of effective communication of key patient information and the quality of handovers. RESULTS: Ninety-three percent of EM residents (50 of 54) and 80% of IM residents (74 of 93) responded to the survey. The EM residents judged their handover performance to be better than how their IM colleagues assessed them on most questions. The IM residents reported that one-half of the time, EM residents provided organized and clear information, whereas EM residents self-reported that they did so most of the time (80%-90%). The IM residents reported that 25% of handovers were suboptimal and resulted in admission to an inappropriate level of care, and 10% led to harm or delay in care. The EM residents reported suboptimal communication was less common (5%). On the global assessment of whether the admission handover provided the information needed for good patient care, IM residents rated the quality of the handover data lower than did responding EM residents. CONCLUSIONS: There are gaps in communicating critical patient information during admission handovers as perceived by EM and IM residents. This information can form the basis for efforts to improve these handovers.

Genomic instability and aging-like phenotype in the absence of mammalian SIRT6.

The Sir2 histone deacetylase functions as a chromatin silencer to regulate recombination, genomic stability, and aging in budding yeast. Seven mammalian Sir2 homologs have been identified (SIRT1-SIRT7), and it has been speculated that some may have similar functions to Sir2. Here, we demonstrate that SIRT6 is a nuclear, chromatin-associated protein that promotes resistance to DNA damage and suppresses genomic instability in mouse cells, in association with a role in base excision repair (BER). SIRT6-deficient mice are small and at 2-3 weeks of age develop abnormalities that include profound lymphopenia, loss of subcutaneous fat, lordokyphosis, and severe metabolic defects, eventually dying at about 4 weeks. We conclude that one function of SIRT6 is to promote normal DNA repair, and that SIRT6 loss leads to abnormalities in mice that overlap with aging-associated degenerative processes.

Mammalian SIRT1 limits replicative life span in response to chronic genotoxic stress.

The Saccharomyces cerevisiae chromatin silencing factor Sir2 suppresses genomic instability and extends replicative life span. In contrast, we find that mouse embryonic fibroblasts (MEFs) deficient for SIRT1, a mammalian Sir2 homolog, have dramatically increased resistance to replicative senescence. Extended replicative life span of SIRT1-deficient MEFs correlates with enhanced proliferative capacity under conditions of chronic, sublethal oxidative stress. In this context, SIRT1-deficient cells fail to normally upregulate either the p19(ARF) senescence regulator or its downstream target p53. However, upon acute DNA damage or oncogene expression, SIRT1-deficient cells show normal p19(ARF) induction and cell cycle arrest. Together, our findings demonstrate an unexpected SIRT1 function in promoting replicative senescence in response to chronic cellular stress and implicate p19(ARF) as a downstream effector in this pathway.