Decreasing Blood Culture Contamination Rates in the Emergency Department

Introduction: Blood cultures (BCs) are a vital diagnostic tool for sepsis in patients with a suspected infection. Emergency departments are the primary place where BCs are drawn, but the BC contamination rates in emergency departments are the highest and most varied in healthcare. This project’s goal was to decrease the BC contamination rate below 3% (the national benchmark for BC contamination) in an ED in the Southeastern region through the implementation of a blood culture collection toolkit. Methods: The best practices for reducing the BC contamination rate in the emergency department was determined through a thorough literature review. A cost-effective, evidence-based plan was formed to utilize emergency department resources more effectively to decrease the BC contamination rate. The BC toolkit consisted of nursing education on proper BC collection, monthly aggregate level feedback in the ED, and packaged BC collection kit. Results: The monthly contamination rates were 3.6%, 1,7%, and 2.1% respectively during the 3-month implementation of the project. This emergency department had not had two consecutive months with contamination rates less than 3% in 3 years prior to this project. When compared to the corresponding 3 months from the previous year, there was a statistically significant decrease in the BC contamination rates during implementation. There was a clinically significant decrease in the BC contamination rates when compared to the 3 months immediately before implementation. Discussion: As evidenced by the results of this project, emergency departments can decrease BC contamination rates to meet the national benchmark of 3% through a well-structured strategy. Further, this can be accomplished at no additional cost to the emergency department. The cost-effective nature of this project combined with a strong sense of teamwork will lead to sustainable change in emergency departments to consistently improve the quality of care given to patients

The long-term evolution of the spin, pulse shape, and orbit of the accretion-powered millisecond pulsar SAX J1808.4-3658

We present a 7 yr timing study of the 2.5 ms X-ray pulsar SAX J1808.4-3658, an X-ray transient with a recurrence time of ~2 yr, using data from the Rossi X-ray Timing Explorer covering 4 transient outbursts (1998-2005). We verify that the 401 Hz pulsation traces the spin frequency fundamental and not a harmonic. Substantial pulse shape variability, both stochastic and systematic, was observed during each outburst. Analysis of the systematic pulse shape changes suggests that, as an outburst dims, the X-ray "hot spot" on the pulsar surface drifts longitudinally and a second hot spot may appear. The overall pulse shape variability limits the ability to measure spin frequency evolution within a given X-ray outburst (and calls previous nudot measurements of this source into question), with typical upper limits of |nudot| < 2.5x10^{-14} Hz/s (2 sigma). However, combining data from all the outbursts shows with high (6 sigma) significance that the pulsar is undergoing long-term spin down at a rate nudot = (-5.6+/-2.0)x10^{-16} Hz/s, with most of the spin evolution occurring during X-ray quiescence. We discuss the possible contributions of magnetic propeller torques, magnetic dipole radiation, and gravitational radiation to the measured spin down, setting an upper limit of B < 1.5x10^8 G for the pulsar's surface dipole magnetic field and and Q/I < 5x10^{-9} for the fractional mass quadrupole moment. We also measured an orbital period derivative of Pdot = (3.5+/-0.2)x10^{-12} s/s. This surprising large Pdot is reminiscent of the large and quasi-cyclic orbital period variation observed in the so-called "black widow" millisecond radio pulsars, supporting speculation that SAX J1808.4-3658 may turn on as a radio pulsar during quiescence. In an appendix we derive an improved (0.15 arcsec) source position from optical data.Comment: 22 pages, 10 figures; accepted for publication in Ap

Insights from wildfire science: A resource for fire policy discussions

Record blazes swept across parts of the US in 2015, burning more than 10 million acres. The four biggest fire seasons since 1960 have all occurred in the last 10 years, leading to fears of a ‘new normal’ for wildfire. Fire fighters and forest managers are overwhelmed, and it is clear that the policy and management approaches of the past will not suffice under this new era of western wildfires. In recent decades, state and federal policymakers, tribes, and others are confronting longer fire seasons (Jolly et al. 2015), more large fires (Dennison et al. 2014), a tripling of homes burned, and a doubling of firefighter deaths (Rasker 2015). Federal agencies now spend $2 to$3 billion annually fighting fires (and in the case of the US Forest Service, over 50% of their budget), and the total cost to society may be up to 30 times more than the direct cost of firefighting. If we want to contain these costs and reduce risks to communities, economies, and natural systems, we can draw on the best available science when designing fire management strategies, as called for in the recent federal report on Wildland Fire Science and Technology. Here, we highlight key science insights that can contribute to the public discourse on wildfire policy and associated management of forests, woodlands, and shrublands. This information is fundamental to decisions that will promote resilient communities and landscapes facing more fire in the future

The Role of APOE4 in Disrupting the Homeostatic Functions of Astrocytes and Microglia in Aging and Alzheimer’s Disease

APOE4 is the greatest genetic risk factor for late-onset Alzheimer’s disease (AD), increasing the risk of developing the disease by 3-fold in the 14% of the population that are carriers. Despite 25 years of research, the exact mechanisms underlying how APOE4 contributes to AD pathogenesis remain incompletely defined. APOE in the brain is primarily expressed by astrocytes and microglia, cell types that are now widely appreciated to play key roles in the pathogenesis of AD; thus, a picture is emerging wherein APOE4 disrupts normal glial cell biology, intersecting with changes that occur during normal aging to ultimately cause neurodegeneration and cognitive dysfunction. This review article will summarize how APOE4 alters specific pathways in astrocytes and microglia in the context of AD and the aging brain. APOE itself, as a secreted lipoprotein without enzymatic activity, may prove challenging to directly target therapeutically in the classical sense. Therefore, a deeper understanding of the underlying pathways responsible for APOE4 toxicity is needed so that more tractable pathways and drug targets can be identified to reduce APOE4-mediated disease risk

Using Nonlinear Response to Estimate the Strength of an Elastic Network

Disordered networks of fragile elastic elements have been proposed as a model of inner porous regions of large bones [Gunaratne et.al., cond-mat/0009221, http://xyz.lanl.gov]. It is shown that the ratio $\Gamma$ of responses of such a network to static and periodic strain can be used to estimate its ultimate (or breaking) stress. Since bone fracture in older adults results from the weakening of porous bone, we discuss the possibility of using $\Gamma$ as a non-invasive diagnostic of osteoporotic bone.Comment: 4 pages, 4 figure

Strength Reduction in Electrical and Elastic Networks

Particular aspects of problems ranging from dielectric breakdown to metal insu- lator transition can be studied using electrical o elastic networks. We present an expression for the mean breakdown strength of such networks.First, we intro- duce a method to evaluate the redistribution of current due to the removal of a finite number of elements from a hyper-cubic network of conducatances.It is used to determine the reduction of breakdown strength due to a fracture of size $\kappa$.Numerical analysis is used to show that the analogous reduction due to random removal of elements from electrical and elastic networks follow a similar form.One possible application, namely the use of bone density as a diagnostic tools for osteorosporosis,is discussed.Comment: one compressed file includes: 9 PostScrpt figures and a text fil

The Spectral Energy Distribution of Powerful Starburst Galaxies I : Modelling the Radio Continuum

This article has been accepted for publication in Monthly Notices of the Royal Astronomical Society. © 2018 The Author(s). Published by Oxford University Press on behalf of the Royal Astronomical Society. All rights reserved.We have acquired radio-continuum data between 70MHz and 48 GHz for a sample of 19 southern starburst galaxies at moderate redshifts (0.067 < z < 0.227) with the aim of separating synchrotron and free-free emission components. Using a Bayesian framework, we find the radio continuum is rarely characterized well by a single power law, instead often exhibiting lowfrequency turnovers below 500 MHz, steepening at mid to high frequencies, and a flattening at high frequencies where free-free emission begins to dominate over the synchrotron emission. These higher order curvature components may be attributed to free-free absorption across multiple regions of star formation with varying optical depths. The decomposed synchrotron and free-free emission components in our sample of galaxies form strong correlations with the total-infrared bolometric luminosities. Finally, we find that without accounting for free-free absorption with turnovers between 90 and 500MHz the radio continuum at low frequency (v < 200 MHz) could be overestimated by upwards of a factor of 12 if a simple power-law extrapolation is used from higher frequencies. The mean synchrotron spectral index of our sample is constrained to be α = -1.06, which is steeper than the canonical value of -0.8 for normal galaxies. We suggest this may be caused by an intrinsically steeper cosmic ray distribution.Peer reviewe

Inflammatory properties of inhibitor of DNA binding 1 secreted by synovial fibroblasts in rheumatoid arthritis

Abstract Background Inhibitor of DNA binding 1 (Id1) is a nuclear protein containing a basic helix-loop-helix (bHLH) domain that regulates cell growth by selective binding and prevention of gene transcription. Sources of Id1 production in rheumatoid arthritis synovial tissue (RA ST) and its range of functional effects in RA remain to be clarified. Methods We analyzed Id1 produced from synovial fibroblasts and endothelial cells (ECs) with histology and real-time polymerase chain reaction (RT-PCR). Fibroblast supernatants subjected to differential centrifugation to isolate and purify exosomes were measured for Id1 by enzyme-linked immunosorbent assay (ELISA). Western blotting of Id1-stimulated ECs was performed to determine the kinetics of intracellular protein phosphorylation. EC intracellular signaling pathways induced by Id1 were subsequently targeted with silencing RNA (siRNA) for angiogenesis inhibition. Results By PCR and histologic analysis, we found that the primary source of Id1 in STs is from activated fibroblasts that correlate with inflammatory scores in human RA ST and in joints from K/BxN serum-induced mice. Normal (NL) and RA synovial fibroblasts increase Id1 production with stimulation by transforming growth factor beta (TGF-β). Most of the Id1 released by RA synovial fibroblasts is contained within exosomes. Endothelial progenitor cells (EPCs) and human dermal microvascular ECs (HMVECs) activate the Jnk signaling pathway in response to Id1, and Jnk siRNA reverses Id1-induced HMVEC vessel formation in Matrigel plugs in vivo. Conclusions Id1 is a pleotropic molecule affecting angiogenesis, vasculogenesis, and fibrosis. Our data shows that Id1 is not only an important nuclear protein, but also can be released from fibroblasts via exosomes. The ability of extracellular Id1 to activate signaling pathways expands the role of Id1 in the orchestration of tissue inflammation.http://deepblue.lib.umich.edu/bitstream/2027.42/134552/1/13075_2016_Article_984.pd

PSRs J0248+6021 and J2240+5832: Young Pulsars in the Northern Galactic Plane. Discovery, Timing, and Gamma-ray observations

Pulsars PSR J0248+6021 (rotation period P=217 ms and spin-down power Edot = 2.13E35 erg/s) and PSR J2240+5832 (P=140 ms, Edot = 2.12E35 erg/s) were discovered in 1997 with the Nancay radio telescope during a northern Galactic plane survey, using the Navy-Berkeley Pulsar Processor (NBPP) filter bank. GeV gamma-ray pulsations from both were discovered using the Fermi Large Area Telescope. Twelve years of radio and polarization data allow detailed investigations. The two pulsars resemble each other both in radio and in gamma-ray data. Both are rare in having a single gamma-ray pulse offset far from the radio peak. The high dispersion measure for PSR J0248+6021 (DM = 370 pc cm^-3) is most likely due to its being within the dense, giant HII region W5 in the Perseus arm at a distance of 2 kpc, not beyond the edge of the Galaxy as obtained from models of average electron distributions. Its high transverse velocity and the low magnetic field along the line-of-sight favor this small distance. Neither gamma-ray, X-ray, nor optical data yield evidence for a pulsar wind nebula surrounding PSR J0248+6021. The gamma-ray luminosity for PSR J0248+6021 is L_ gamma = (1.4 \pm 0.3)\times 10^34 erg/s. For PSR J2240+5832, we find either L_gamma = (7.9 \pm 5.2) \times 10^34 erg/s if the pulsar is in the Outer arm, or L_gamma = (2.2 \pm 1.7) \times 10^34 erg/s for the Perseus arm. These luminosities are consistent with an L_gamma ~ sqrt(Edot) rule. Comparison of the gamma-ray pulse profiles with model predictions, including the constraints obtained from radio polarization data, favor emission in the far magnetosphere. These two pulsars differ mainly in their inclination angles and acceleration gap widths, which in turn explains the observed differences in the gamma-ray peak widths.Comment: 13 pages, Accepted to Astronomy & Astrophysic