4,652 research outputs found

    Ultrasound by emergency physicians to detect abdominal aortic aneurysms: a UK case series

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    Early identification of abdominal aortic aneurysms in some patients can be difficult and the diagnosis is missed in up to 30% of patients. Ultrasound cannot be used to identify a leak, but the presence of an aneurysm in an unstable patient is conclusive. With minimal training emergency physicians can easily identify the aorta and thus in the early phase of resuscitation an aneurysm can be confidently excluded. The purpose of the examination is not to delineate the extent of the aneurysm, but to identify those patients that will need emergency surgery. A series of patients presented to the department in an unstable condition with equivocal abdominal signs. An ultrasound scan in the resuscitation room by members of the emergency department revealed an aneurysm, which was enough to convince the vascular surgeons to take the patient straight to theatre with good results. In patients who are stable, computed tomography will continue to be used to evaluate the extent of the aneurysm and identify a leak

    Distributional fixed point equations for island nucleation in one dimension: a retrospective approach for capture zone scaling

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    The distributions of inter-island gaps and captures zones for islands nucleated on a one-dimensional substrate during submonolayer deposition are considered using a novel retrospective view. This provides an alternative perspective on why scaling occurs in this continuously evolving system. Distributional fixed point equations for the gaps are derived both with and without a mean field approximation for nearest neighbour gap size correlation. Solutions to the equations show that correct consideration of fragmentation bias justifies the mean field approach which can be extended to provide closed-from equations for the capture zones. Our results compare favourably to Monte Carlo data for both point and extended islands using a range of critical island size i=0,1,2,3i=0,1,2,3. We also find satisfactory agreement with theoretical models based on more traditional fragmentation theory approaches.Comment: 9 pages, 7 figures and 1 tabl

    Crossover in the scaling of island size and capture zone distributions

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    Simulations of irreversible growth of extended (fractal and square) islands with critical island sizes i=1 and 2 are performed in broad ranges of coverage \theta and diffusion-to-deposition ratios R in order to investigate scaling of island size and capture zone area distributions (ISD, CZD). Large \theta and small R lead to a crossover from the CZD predicted by the theory of Pimpinelli and Einstein (PE), with Gaussian right tail, to CZD with simple exponential decays. The corresponding ISD also cross over from Gaussian or faster decays to simple exponential ones. For fractal islands, these features are explained by changes in the island growth kinetics, from a competition for capture of diffusing adatoms (PE scaling) to aggregation of adatoms with effectively irrelevant diffusion, which is characteristic of random sequential adsorption (RSA) without surface diffusion. This interpretation is confirmed by studying the crossover with similar CZ areas (of order 100 sites) in a model with freezing of diffusing adatoms that corresponds to i=0. For square islands, deviations from PE predictions appear for coverages near \theta=0.2 and are mainly related to island coalescence. Our results show that the range of applicability of the PE theory is narrow, thus observing the predicted Gaussian tail of CZD may be difficult in real systems.Comment: 9 pages, 7 figure

    Asymptotic Capture-Number and Island-Size Distributions for One-Dimensional Irreversible Submonolayer Growth

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    Using a set of evolution equations [J.G. Amar {\it et al}, Phys. Rev. Lett. {\bf 86}, 3092 (2001)] for the average gap-size between islands, we calculate analytically the asymptotic scaled capture-number distribution (CND) for one-dimensional irreversible submonolayer growth of point islands. The predicted asymptotic CND is in reasonably good agreement with kinetic Monte-Carlo (KMC) results and leads to a \textit{non-divergent asymptotic} scaled island-size distribution (ISD). We then show that a slight modification of our analytical form leads to an analytic expression for the asymptotic CND and a resulting asymptotic ISD which are in excellent agreement with KMC simulations. We also show that in the asymptotic limit the self-averaging property of the capture zones holds exactly while the asymptotic scaled gap distribution is equal to the scaled CND.Comment: 4 pages, 1 figure, submitted to Phys. Rev.

    Capture-zone scaling in island nucleation: phenomenological theory of an example of universal fluctuation behavior

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    In studies of island nucleation and growth, the distribution of capture zones, essentially proximity cells, can give more insight than island-size distributions. In contrast to the complicated expressions, ad hoc or derived from rate equations, usually used, we find the capture-zone distribution can be described by a simple expression generalizing the Wigner surmise from random matrix theory that accounts for the distribution of spacings in a host of fluctuation phenomena. Furthermore, its single adjustable parameter can be simply related to the critical nucleus of growth models and the substrate dimensionality. We compare with extensive published kinetic Monte Carlo data and limited experimental data. A phenomenological theory sheds light on the result.Comment: 5 pages, 4 figures, originally submitted to Phys. Rev. Lett. on Dec. 15, 2006; revised version v2 tightens and focuses the presentation, emphasizes the importance of universal features of fluctuations, corrects an error for d=1, replaces 2 of the figure

    Spatio-temporal distribution of nucleation events during crystal growth

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    We consider irreversible second-layer nucleation that occurs when two adatoms on a terrace meet. We solve the problem analytically in one dimension for zero and infinite step-edge barriers, and numerically for any value of the barriers in one and two dimensions. For large barriers, the spatial distribution of nucleation events strongly differs from ρ2\rho^2, where ρ\rho is the stationary adatom density in the presence of a constant flux. The probability Q(t)Q(t) that nucleation occurs at time tt after the deposition of the second adatom, decays for short time as a power law [Q(t)t1/2Q(t)\sim t^{-1/2}] in d=1d=1 and logarithmically [Q(t)1/ln(t/t0)Q(t)\sim 1/\ln(t/t_0)] in d=2d=2; for long time it decays exponentially. Theories of the nucleation rate ω\omega based on the assumption that it is proportional to ρ2\rho^2 are shown to overestimate ω\omega by a factor proportional to the number of times an adatom diffusing on the terrace visits an already visited lattice site.Comment: 4 pages, 3 figures; accepted for publication on PR

    Island nucleation in the presence of step edge barriers: Theory and applications

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    We develop a theory of nucleation on top of two-dimensional islands bordered by steps with an additional energy barrier ΔES\Delta E_S for descending atoms. The theory is based on the concept of the residence time of an adatom on the island,and yields an expression for the nucleation rate which becomes exact in the limit of strong step edge barriers. This expression differs qualitatively and quantitatively from that obtained using the conventional rate equation approach to nucleation [J. Tersoff et al., Phys. Rev. Lett.72, 266 (1994)]. We argue that rate equation theory fails because nucleation is dominated by the rare instances when two atoms are present on the island simultaneously. The theory is applied to two distinct problems: The onset of second layer nucleation in submonolayer growth, and the distribution of the sizes of top terraces of multilayer mounds under conditions of strong step edge barriers. Application to homoepitaxial growth on Pt(111) yields the estimate ΔES0.33\Delta E_S \geq 0.33 eV for the additional energy barrier at CO-decorated steps.Comment: 13 pages, 3 figure

    Expression of citrulline and homocitrulline residues in the lungs of non-smokers and smokers : implications for autoimmunity in rheumatoid arthritis

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    Introduction: Smoking is a well-established risk factor for rheumatoid arthritis (RA), and it has been proposed that smoking-induced citrullination renders autoantigens immunogenic. To investigate this mechanism, we examined human lung tissue from 40 subjects with defined smoking status, with or without chronic obstructive pulmonary disease (COPD), and control tissues from other organs for citrullinated proteins and the deiminating enzymes peptidylarginine deiminase type-2 (PAD2) and -4 (PAD4). Methods: Lung tissue samples, dissected from lobectomy specimens from 10 never smokers, 10 smokers without airflow limitation, 13 COPD smokers and eight COPD ex-smokers, and control tissue samples (spleen, skeletal muscle, liver, ovary, lymph node, kidney and heart), were analysed for citrullinated proteins, PAD2 and PAD4 by immunoblotting. Citrulline and homocitrulline residues in enolase and vimentin were analysed by partial purification by gel electrophoresis followed by mass spectrometry in 12 of the lung samples and one from each control tissues. Band intensities were scored semi-quantitatively and analysed by two-tailed Mann-Whitney T-test. Results: Within the lung tissue samples, citrullinated proteins, PAD2 and PAD4 were found in all samples, with an increase in citrullination in COPD (P = 0.039), but minimal difference between smokers and non-smokers (P = 0.77). Citrullination was also detected at lower levels in the tissues from other organs, principally in lymph node, kidney and skeletal muscle. Mass spectrometry of the lung samples showed that vimentin was citrullinated at positions 71, 304, 346, 410 and 450 in non-smokers and smokers both with and without COPD. A homocitrulline at position 104 was found in four out of six COPD samples and one out of six non-COPD. Citrulline-450 was also found in three of the control tissues. There were no citrulline or homocitrulline residues demonstrated in a-enolase. Conclusions: We have shown evidence of citrullination of vimentin, a major autoantigen in RA, in both non-smokers and smokers. The increase in citrullinated proteins in COPD suggests that citrullination in the lungs of smokers is mainly due to inflammation. The ubiquity of citrullination of vimentin in the lungs and other tissues suggests that the relationship between smoking and autoimmunity in RA may be more complex than previously thought
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