2,164 research outputs found

    Left Superior Pulmonary Vein Rhythm Masquerading as Sinus Rhythm

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    Rajiv Mahajan, Han S. Lim, Dennis H. Lau, Prashanthan Sander

    A method for encoding clinical datasets with SNOMED CT

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    <p>Abstract</p> <p>Background</p> <p>Over the past decade there has been a growing body of literature on how the Systematised Nomenclature of Medicine Clinical Terms (SNOMED CT) can be implemented and used in different clinical settings. Yet, for those charged with incorporating SNOMED CT into their organisation's clinical applications and vocabulary systems, there are few detailed encoding instructions and examples available to show how this can be done and the issues involved. This paper describes a heuristic method that can be used to encode clinical terms in SNOMED CT and an illustration of how it was applied to encode an existing palliative care dataset.</p> <p>Methods</p> <p>The encoding process involves: identifying input data items; cleaning the data items; encoding the cleaned data items; and exporting the encoded terms as output term sets. Four outputs are produced: the SNOMED CT reference set; interface terminology set; SNOMED CT extension set and unencodeable term set.</p> <p>Results</p> <p>The original palliative care database contained 211 data elements, 145 coded values and 37,248 free text values. We were able to encode ~84% of the terms, another ~8% require further encoding and verification while terms that had a frequency of fewer than five were not encoded (~7%).</p> <p>Conclusions</p> <p>From the pilot, it would seem our SNOMED CT encoding method has the potential to become a general purpose terminology encoding approach that can be used in different clinical systems.</p

    Pseudomonas aeruginosa Elastase Provides an Escape from Phagocytosis by Degrading the Pulmonary Surfactant Protein-A

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    Pseudomonas aeruginosa is an opportunistic pathogen that causes both acute pneumonitis in immunocompromised patients and chronic lung infections in individuals with cystic fibrosis and other bronchiectasis. Over 75% of clinical isolates of P. aeruginosa secrete elastase B (LasB), an elastolytic metalloproteinase that is encoded by the lasB gene. Previously, in vitro studies have demonstrated that LasB degrades a number of components in both the innate and adaptive immune systems. These include surfactant proteins, antibacterial peptides, cytokines, chemokines and immunoglobulins. However, the contribution of LasB to lung infection by P. aeruginosa and to inactivation of pulmonary innate immunity in vivo needs more clarification. In this study, we examined the mechanisms underlying enhanced clearance of the ΔlasB mutant in mouse lungs. The ΔlasB mutant was attenuated in virulence when compared to the wild-type strain PAO1 during lung infection in SP-A+/+ mice. However, the ΔlasB mutant was as virulent as PAO1 in the lungs of SP-A-/- mice. Detailed analysis showed that the ΔlasB mutant was more susceptible to SP-A-mediated opsonization but not membrane permeabilization. In vitroand in vivo phagocytosis experiments revealed that SP-A augmented the phagocytosis of ΔlasB mutant bacteria more efficiently than the isogenic wild-type PAO1. The ΔlasB mutant was found to have a severely reduced ability to degrade SP-A, consequently making it unable to evade opsonization by the collectin during phagocytosis. These results suggest that P. aeruginosa LasB protects against SP-A-mediated opsonization by degrading the collectin

    Shaken and stirred: conduction and turbulence in clusters of galaxies

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    (abridged) Uninhibited radiative cooling in clusters of galaxies would lead to excessive mass accretion rates contrary to observations. One of the key proposals to offset radiative energy losses is thermal conduction from outer, hotter layers of cool core clusters to their centers. However, conduction is sensitive to magnetic field topology. In cool-core clusters the heat buoyancy instability (HBI) leads to B-fields ordered preferentially in the direction perpendicular to that of gravity, which significantly reduces the level of conduction below the classical Spitzer-Braginskii value. However, the cluster cool cores are rarely in perfect hydrostatic equilibrium. Sloshing motions due to minor mergers, galaxy motions or AGN can significantly perturb the gas and affect the level of thermal conduction. We perform 3D AMR MHD simulations of the effect of turbulence on the properties of the anisotropic thermal conduction in cool core clusters. We show that very weak subsonic motions, well within observational constraints, can randomize the magnetic field and significantly boost effective thermal conduction beyond the saturated values expected in the pure unperturbed HBI case. We find that the turbulent motions can essentially restore the conductive heat flow to the cool core to level comparable to the theoretical maximum of 1/3 Spitzer for a highly tangled field. Runs with radiative cooling show that the cooling catastrophe can be averted and the cluster core stabilized. Above a critical Froude number, these same turbulent motions also eliminate the tangential bias in the velocity and magnetic field that is otherwise induced by the trapped g-modes. Our results can be tested with future radio polarization measurements, and have implications for efficient metal dispersal in clusters.Comment: submitted to ApJ, references added, expanded Section

    A profile of the online dissemination of national influenza surveillance data

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    <p>Abstract</p> <p>Background</p> <p>Influenza surveillance systems provide important and timely information to health service providers on trends in the circulation of influenza virus and other upper respiratory tract infections. Online dissemination of surveillance data is useful for risk communication to health care professionals, the media and the general public. We reviewed national influenza surveillance websites from around the world to describe the main features of surveillance data dissemination.</p> <p>Methods</p> <p>We searched for national influenza surveillance websites for every country and reviewed the resulting sites where available during the period from November 2008 through February 2009. Literature about influenza surveillance was searched at MEDLINE for relevant hyperlinks to related websites. Non-English websites were translated into English using human translators or Google language tools.</p> <p>Results</p> <p>A total of 70 national influenza surveillance websites were identified. The percentage of developing countries with surveillance websites was lower than that of developed countries (22% versus 57% respectively). Most of the websites (74%) were in English or provided an English version. The most common surveillance methods included influenza-like illness consultation rates in primary care settings (89%) and laboratory surveillance (44%). Most websites (70%) provided data within a static report format and 66% of the websites provided data with at least weekly resolution.</p> <p>Conclusion</p> <p>Appropriate dissemination of surveillance data is important to maximize the utility of collected data. There may be room for improvement in the style and content of the dissemination of influenza data to health care professionals and the general public.</p

    The Anti-Sigma Factor MucA of Pseudomonas aeruginosa: Dramatic Differences of a mucA22 vs. a ΔmucA Mutant in Anaerobic Acidified Nitrite Sensitivity of Planktonic and Biofilm Bacteria in vitro and During Chronic Murine Lung Infection

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    Mucoid mucA22 Pseudomonas aeruginosa (PA) is an opportunistic lung pathogen of cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) patients that is highly sensitive to acidified nitrite (A-NO2-). In this study, we first screened PA mutant strains for sensitivity or resistance to 20 mM A-NO2- under anaerobic conditions that represent the chronic stages of the aforementioned diseases. Mutants found to be sensitive to A-NO2- included PA0964 (pmpR, PQS biosynthesis), PA4455 (probable ABC transporter permease), katA (major catalase, KatA) and rhlR (quorum sensing regulator). In contrast, mutants lacking PA0450 (a putative phosphate transporter) and PA1505 (moaA2) were A-NO2- resistant. However, we were puzzled when we discovered that mucA22 mutant bacteria, a frequently isolated mucA allele in CF and to a lesser extent COPD, were more sensitive to A-NO2- than a truncated ΔmucA deletion (Δ157–194) mutant in planktonic and biofilm culture, as well as during a chronic murine lung infection. Subsequent transcriptional profiling of anaerobic, A-NO2--treated bacteria revealed restoration of near wild-type transcript levels of protective NO2- and nitric oxide (NO) reductase (nirS and norCB, respectively) in the ΔmucA mutant in contrast to extremely low levels in the A-NO2--sensitive mucA22 mutant. Proteins that were S-nitrosylated by NO derived from A-NO2- reduction in the sensitive mucA22 strain were those involved in anaerobic respiration (NirQ, NirS), pyruvate fermentation (UspK), global gene regulation (Vfr), the TCA cycle (succinate dehydrogenase, SdhB) and several double mutants were even more sensitive to A-NO2-. Bioinformatic-based data point to future studies designed to elucidate potential cellular binding partners for MucA and MucA22. Given that A-NO2- is a potentially viable treatment strategy to combat PA and other infections, this study offers novel developments as to how clinicians might better treat problematic PA infections in COPD and CF airway diseases

    Adaptively refined large eddy simulations of clusters

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    We present a numerical scheme for modelling unresolved turbulence in cosmological adaptive mesh refinement codes. As a first application, we study the evolution of turbulence in the intra-cluster medium and in the core of a galaxy cluster. Simulations with and without subgrid scale model are compared in detail. Since the flow in the ICM is subsonic, the global turbulent energy contribution at the unresolved length scales is smaller than 1% of the internal energy. We find that the production of turbulence is closely correlated with merger events occurring in the cluster environment, and its dissipation locally affects the cluster energy budget. Because of this additional source of dissipation, the core temperature is larger and the density is smaller in the presence of subgrid scale turbulence than in the standard adiabatic run, resulting in a higher entropy core value.Comment: Submitted to ApJ, 14 pages, 14 figures, 3 table

    Pharmacological inhibition of sodium-proton-exchanger subtype 3-mediated sodium absorption in the gut reduces atrial fibrillation susceptibility in obese spontaneously hypertensive rats

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    Background: Increased sodium uptake has been shown to contribute to hypertension and cardiac endorgan damage. The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal sodium absorption. Whether a reduction in intestinal sodium absorption can prevent the development of an atrial arrhythmogenic substrate in hypertension is unknown. Methods: Eight-week-old obese spontaneously hypertensive rats (SHR-ob) were treated for six weeks with the gut-specific NHE3-inhibitor SAR (1-(beta-D-glucopyranosyl)-3-{3-[(4S)-6,8-dichloro-2-methyl-1, 2,3,4-tetrahydroiso-chinolin-4-yl]phenyl}urea, 1 mg/kg/d in chow, SHR-ob SAR, n = 7) and compared to aged-matched placebo-treated SHR-ob (SHR-ob PLAC, n = 8). Cardiac magnetic resonance imaging was performed at the end of the treatment period to assess atrial emptying function. Afterwards, local conduction disturbances and inducible atrial fibrillation (AF) duration were determined and histological analysis to quantify atrial fibrosis amount were performed. Results: Inhibition of intestinal NHE3 by SAR increased fecal sodium excretion, resulted in marked changes in feces electrolyte concentrations and water content, reduced blood pressure and preserved atrial emptying function (active total percent emptying: SHR-ob SAR: 0.47 +/- 0.05% vs. SHR-ob PLAC: 0.38 +/- 0.007, p <0.0001). Atrial fibrosis content was lower (21.4 +/- 2.5% vs. 36.7 +/- 1.2%, p <0.0001) and areas of slow conduction were smaller (2.5 +/- 0.09% vs. 5.3 +/- 0.2%, p <0.0001) in SHR-ob SAR compared to SHR-ob PLAC. Left atrial burst stimulation resulted in shorter inducible AF-durations in SHR-ob SAR compared to SHR-ob PLAC. Conclusions: Reduction of intestinal sodium absorption and subsequent changes in feces milieu by pharmacological NHE3 inhibition in the gut preserved atrial emptying function and reduced AF susceptibility. Whether pharmacological NHE3 inhibition in the gut prevents AF in humans warrants further study. (C) 2020 The Authors. Published by Elsevier B.V
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