Continuous Physiological Monitoring Improves Patient Outcomes.

BACKGROUND: General patient acuity is increasing in the United States, with more patients having multiple comorbidities and acute-on-chronic conditions. Hospitalizations may also be complicated by serious adverse events, often unrelated to the admitting medical diagnosis. In our facility, the late detection of patient deterioration on general medical units often resulted in increased length of stay (LOS) in the ICU and poor patient outcomes. PURPOSE: The purpose of this project was to improve patient surveillance and better identify early signs of patient deterioration through the use of continuous vital sign monitoring technology. METHODS: To improve detection of patient deterioration, a nurse-led monitoring and response system was developed using a wearable, wireless device for continuous vital sign surveillance. The patient data the device provided was used with early warning scores and sepsis screening protocols for timely goal-directed interventions. RESULTS: Ninety-seven percent of patient deterioration events were recognized and treated as a result of this continuous monitoring and response system. Rapid response team activations decreased by 53% between baseline and the intervention period. LOS among patients transferred to the ICU decreased from 2.82 to 2.19 days. Nurse satisfaction with use of the continuous monitoring device was positive, with 74% of nurses surveyed reporting that information provided by the device enhanced decision-making. CONCLUSIONS: New technology for patient surveillance, in this case a nurse-led monitoring and response system, can be successfully integrated into general care practice. Use of the nurse-led response system helped nurses recognize early signs of deterioration and continue meaningful patient interactions.

UNC-120/SRF independently controls muscle aging and lifespan in Caenorhabditis elegans.

Aging is commonly defined as the loss of global homeostasis, which results from progressive alteration of all organs function. This model is currently challenged by recent data showing that interventions that extend lifespan do not always increase the overall fitness of the organism. These data suggest the existence of tissue-specific factors that regulate the pace of aging in a cell-autonomous manner. Here, we investigated aging of Caenorhabditis elegans striated muscles at the subcellular and the physiological level. Our data show that muscle aging is characterized by a dramatic decrease in the expression of genes encoding proteins required for muscle contraction, followed by a change in mitochondria morphology, and an increase in autophagosome number. Myofilaments, however, remain unaffected during aging. We demonstrated that the conserved transcription factor UNC-120/SRF regulates muscle aging biomarkers. Interestingly, the role of UNC-120/SRF in the control of muscle aging can be dissociated from its broader effect on lifespan. In daf-2/insulin/IGF1 receptor mutants, which exhibit a delayed appearance of muscle aging biomarkers and are long-lived, disruption of unc-120 accelerates muscle aging but does not suppress the lifespan phenotype of daf-2 mutant. Conversely, unc-120 overexpression delays muscle aging but does not increase lifespan. Overall, we demonstrate that UNC-120/SRF controls the pace of muscle aging in a cell-autonomous manner downstream of the insulin/IGF1 receptor.

Ultra-structural time-course study in the C. elegans model for Duchenne muscular dystrophy highlights a crucial role for sarcomere-anchoring structures and sarcolemma integrity in the earliest steps of the muscle degeneration process.

Duchenne muscular dystrophy (DMD) is a genetic disease characterized by progressive muscle degeneration due to mutations in the dystrophin gene. In spite of great advances in the design of curative treatments, most patients currently receive palliative therapies with steroid molecules such as prednisone or deflazacort thought to act through their immunosuppressive properties. These molecules only slightly slow down the progression of the disease and lead to severe side effects. Fundamental research is still needed to reveal the mechanisms involved in the disease that could be exploited as therapeutic targets. By studying a Caenorhabditis elegans model for DMD, we show here that dystrophin-dependent muscle degeneration is likely to be cell autonomous and affects the muscle cells the most involved in locomotion. We demonstrate that muscle degeneration is dependent on exercise and force production. Exhaustive studies by electron microscopy allowed establishing for the first time the chronology of subcellular events occurring during the entire process of muscle degeneration. This chronology highlighted the crucial role for dystrophin in stabilizing sarcomeric anchoring structures and the sarcolemma. Our results suggest that the disruption of sarcomeric anchoring structures and sarcolemma integrity, observed at the onset of the muscle degeneration process, triggers subcellular consequences that lead to muscle cell death. An ultra-structural analysis of muscle biopsies from DMD patients suggested that the chronology of subcellular events established in C. elegans models the pathogenesis in human. Finally, we found that the loss of sarcolemma integrity was greatly reduced after prednisone treatment suggesting a role for this molecule in plasma membrane stabilization.