Effects of Noise Reduction and Care Clustering on Quality of Sleep in Critical Care Patients

Introduction: Sleep deprivation has detrimental effects on critical patients’ health. A lack of sleep can affect multiple body systems. There are nursing interventions that can reduce sleep deprivation. However, there is inconclusive evidence on how to properly assess sleep deprivation and implement sleep promoting nursing interventions in clinical practice. Purpose: The purpose of this literature review is to examine the effects of noise reduction and nursing care clustering on improving the quality of patient sleep in the critical care setting. Methods: This literature review was conducted using 10 sources published within the last 5 years. Inclusion criteria consisted of articles about the effects of noise, quality of sleep, and implementation of nurse care clustering on various critical care populations. The 6 databases used for this research were UpToDate, CINAHL, PubMed, PsycInfo, Proquest, and CCForum. This research concentrated on examining articles containing nursing interventions for noise reduction and care clustering related to quality of sleep. Results: Noise has a negative effect on sleep by causing more arousals/awakenings, which greatly impacts the restorative function of the process. Noise is not the only sleep disturbing factor, but it has been shown to be significant. Some noise sources cannot be eliminated due to safety reasons, but interventions exist to help counteract the effects of noise. Nursing care interventions are as disruptive to sleep as noise. 13.9% of nursing interruptions could be safely omitted, and nurses should cluster care to promote sleep. Interventions to prevent sleep disruption can be practical in routine nursing, but nurses are less likely to implement them at night because prioritizing care clustering can require more time and effort. Discussion: Sleep deprivation causes major health concerns in critical care patients. Noise and nursing care interventions have been found to cause equal disruptions in sleep. Noise reduction and care clustering have been observed to reduce sleep deprivation. Further evidence is needed on how to effectively and practically implement these nursing interventions into daily nursing practice

Pathobiology and Treatment of Hepatitis Virus-Related Thrombocytopenia

Thrombocytopenia is a well recognized complication of infections, including those from hepatotropic viruses. Thrombocytopenia may actually be the only manifestation of vital hepatitis, which should therefore be considered in the differential diagnosis of primary immune thrombocytopenia (ITP). The mechanisms of thrombocytopenia associated with viral hepatitis vary widely depending on the specific infectious agent and the severity of liver disease. Most of the studies have described thrombocytopenia in association with chronic hepatitis C virus (HCV) infection, the most common cause of chronic infection worldwide. Studies have shown that treatment of HCV infection often results in substantial improvement or complete recovery of the thrombocytopenia. In patients with thrombocytopenia associated with HCV-related chronic liver disease, the use of eltrombopag, a thrombopoietin receptor agonist, normalizes platelet levels thereby permitting the initiation of antiviral therapy

On Coding for Reliable Communication over Packet Networks

We present a capacity-achieving coding scheme for unicast or multicast over lossy packet networks. In the scheme, intermediate nodes perform additional coding yet do not decode nor even wait for a block of packets before sending out coded packets. Rather, whenever they have a transmission opportunity, they send out coded packets formed from random linear combinations of previously received packets. All coding and decoding operations have polynomial complexity. We show that the scheme is capacity-achieving as long as packets received on a link arrive according to a process that has an average rate. Thus, packet losses on a link may exhibit correlation in time or with losses on other links. In the special case of Poisson traffic with i.i.d. losses, we give error exponents that quantify the rate of decay of the probability of error with coding delay. Our analysis of the scheme shows that it is not only capacity-achieving, but that the propagation of packets carrying "innovative" information follows the propagation of jobs through a queueing network, and therefore fluid flow models yield good approximations. We consider networks with both lossy point-to-point and broadcast links, allowing us to model both wireline and wireless packet networks.Comment: 33 pages, 6 figures; revised appendi

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes

publisher: Elsevier articletitle: Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes journaltitle: Cell articlelink: https://doi.org/10.1016/j.cell.2018.05.046 content_type: article copyright: © 2018 Elsevier Inc

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)