167 resultados para Upper airway collapse


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The emission measure distribution in the upper transition region and corona of e Eri is derived from observed emission-line fluxes. Theoretical emission measure distributions are calculated assuming that the radiation losses are balanced by the net conductive flux. We discuss how the area factor of the emitting regions as a function of temperature can be derived from a comparison between these emission measure distributions. It is found that the filling factor varies from ~0.2 in the mid-transition region to ~1.0 in the inner corona. The sensitivity of these results to the adopted ion fractions, the iron abundance and other parameters is discussed. The area factors found are qualitatively similar to the observed structure of the solar atmosphere, and can be used to constrain two-component models of the chromosphere. Given further observations, the method could be applied to investigate the trends in filling factors with indicators of stellar activity.

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Outer membrane protein A (OmpA) is a class of proteins highly conserved among the Enterobacteriaceae family and throughout evolution. Klebsiella pneumoniae is a capsulated Gram-negative pathogen. It is an important cause of community-acquired and nosocomial pneumonia. Evidence indicates that K. pneumoniae infections are characterized by a lack of an early inflammatory response. Data from our laboratory indicate that K. pneumoniae CPS helps to suppress the host inflammatory response. However, it is unknown whether K. pneumoniae employs additional factors to modulate host inflammatory responses. Here, we report that K. pneumoniae OmpA is important for immune evasion in vitro and in vivo. Infection of A549 and normal human bronchial cells with 52OmpA2, an ompA mutant, increased the levels of IL-8. 52145-?wca ompA, which does not express CPS and ompA, induced the highest levels of IL-8. Both mutants could be complemented. In vivo, 52OmpA2 induced higher levels of tnfa, kc, and il6 than the wild type. ompA mutants activated NF-?B, and the phosphorylation of p38, p44/42, and JNK MAPKs and IL-8 induction was via NF-?B-dependent and p38- and p44/42-dependent pathways. 52OmpA2 engaged TLR2 and -4 to activate NF-?B, whereas 52145-?wca ompA activated not only TLR2 and TLR4 but also NOD1. Finally, we demonstrate that the ompA mutant is attenuated in the pneumonia mouse model. The results of this study indicate that K. pneumoniae OmpA contributes to attenuate airway cell responses. This may facilitate pathogen survival in the hostile environment of the lung. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

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Klebsiella pneumoniae is a capsulated Gram negative bacterial pathogen and a frequent cause of nosocomial infections. Despite its clinical relevance, little is known about the features of the interaction between K. pneumoniae and lung epithelial cells on a cellular level, neither about the role of capsule polysaccharide, one of its best characterised virulence factors, in this interaction.

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Airway epithelial cells act as the first barrier against pathogens. These cells recognize conserved structural motifs expressed by microbial pathogens via Toll-like receptors (TLRs) expressed on the surface. In contrast to the level of expression in lymphoid cells, the level of expression of TLR2 and TLR4 in airway epithelial cells is low under physiological conditions. Here we explored whether Klebsiella pneumoniae upregulates the expression of TLRs in human airway epithelial cells. We found that the expression of TLR2 and TLR4 by A549 cells and human primary airway cells was upregulated upon infection with K. pneumoniae. The increased expression of TLRs resulted in enhancement of the cellular response upon stimulation with Pam3CSK4 and lipopolysaccharide, which are TLR2 and TLR4 agonists, respectively. Klebsiella-dependent upregulation of TLR expression occurred via a positive IkappaBalpha-dependent NF-kappaBeta pathway and via negative p38 and p44/42 mitogen-activated protein kinase-dependent pathways. We showed that Klebsiella-induced TLR2 and TLR4 upregulation was dependent on TLR activation. An isogenic capsule polysaccharide (CPS) mutant did not increase TLR2 and TLR4 expression. Purified CPS upregulated TLR2 and TLR4 expression, and polymyxin B did not abrogate CPS-induced TLR upregulation. Although no proteins were detected in the CPS preparation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and colloidal gold staining, we could not rule out the possibility that traces of protein in our CPS preparation could have been responsible, at least in part, for the TLR upregulation.

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The means by which airway epithelial cells sense a bacterial infection and which intracellular signalling pathways are activated upon infection are poorly understood. A549 cells and human primary airway cells (NHBE) were used to investigate the response to infection with Klebsiella pneumoniae. Infection of A549 and NHBE with K. pneumoniae 52K10, a capsule polysaccharide (CPS) mutant, increased the surface levels of ICAM-1 and caused the release of IL-8. By contrast, the wild-type strain did not elicit these responses. Consistent with a functional role for these responses, there was a correlation between ICAM-1 levels and the number of adherent leukocytes on the epithelial cell surface. In addition, treatment of neutrophils with IL-8 enhanced their ability to kill K. pneumoniae. Strain 52K10 was internalized by A549 cells more efficiently than the wild-type, and when infections with 52K10 were performed in the presence of cytochalasin D the inflammatory response was abrogated. These findings suggest that cellular activation is mediated by bacterial internalization and that CPS prevents the activation through the blockage of bacterial adhesion and uptake. Collectively, the results indicate that bacterial internalization by airway epithelial cells could be the triggering signal for the activation of the innate immune system of the airway. Infection of A549 cells by 52K10 was shown to trigger the nuclear translocation of NF-kappaB. Evidence is presented showing that 52K10 activated IL-8 production through Toll-like receptor (TLR) 2 and TLR4 pathways and that A549 cells could use soluble CD14 as TLR co-receptor.

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Although respiratory syncytial virus (RSV) is a major human respiratory pathogen, our knowledge of how it causes disease in humans is limited. Airway epithelial cells are the primary targets of RSV infection in vivo, so the generation and exploitation of RSV infection models based on morphologically and physiologically authentic well-differentiated primary human airway epithelial cells cultured at an air-liquid interface (WD-PAECs) provide timely developments that will help to bridge this gap. Here we review the interaction of RSV with WD-PAEC cultures, the authenticity of the RSV-WD-PAEC models relative to RSV infection of human airway epithelium in vivo, and future directions for their exploitation in our quest to understand RSV pathogenesis in humans.

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Recovery of upper limb function after stroke is poor. The acute to subacute phase after stroke is the optimal time window to promote the recovery of upper limb function. The dose and content of training provided conventionally during this phase is however, unlikely to be adequate to drive functional recovery, especially in the presence of severe motor disability. The current study concerns an approach to address this shortcoming, through evaluation of the SMART Arm, a non-robotic device that enables intensive and repetitive practice of reaching by stroke survivors with severe upper limb disability, with the aim of improving upper limb function. The outcomes of SMART Arm training with or without outcome-triggered electrical stimulation (OT-stim) to augment movement and usual therapy will be compared to usual therapy alone.

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We present observations of the interacting transient SN 2009ip, from the start of the outburst in October 2012 until the end of the 2012 observing season. The transient reached a peak of $M_V$=-17.7 mag before fading rapidly, with a total integrated luminosity of 1.9$\times10^{49}$ erg over the period of August-December 2012. The optical and near infrared spectra are dominated by narrow emission lines, signaling a dense circumstellar environment, together with multiple components of broad emission and absorption in H and He at velocities between 0.5-1.2$\times10^4$ km s$^{-1}$\. We see no evidence for nucleosynthesized material in SN 2009ip, even in late-time pseudo-nebular spectra. We set a limit of $

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1. Lough Neagh is one of the most important non-estuarine sites in the British Isles for overwinteringwildfowl. A change in the waterbird assemblage following the winter of 2000/2001 was drivenmainly by a rapid decline in the population of overwintering diving ducks. Sudden and discretechanges in resident as well as migratory waterbirds may suggest an intrinsic cause.
2. We compared the density and biomass of benthic macroinvertebrates, the food of overwinteringdiving ducks, in 2010 (following the diving duck population decline) with values from a baselinesurvey conducted in 1997/1998 (before the decline in diving ducks).
3. The mean total density of macroinvertebrates declined significantly by c. 65% from 15 300 m2in1997/1998 to 5136 m2in 2010. There was a concomitant c. 70% decline in mean macroinvertebratebiomass from 15 667 mg m2to 5112 mg m2. In terms of taxonomic composition, the relativecontribution of Tanypodinae, Glyptotendipes spp . and Tanytarsini declined, while the relativecontribution of Chironomus spp. increased.
4. We describe a shift in chlorophyll-a concentration, a proxy of phytoplankton biomass, in thelargest freshwater lake in the British Isles coincident with a significant reduction in macroinverte-brate density and biomass, with potential implications for ecosystem processes and ecologically andeconomically important consumer populations, including waterbirds and fishes