Although airway inflammation is recognized as a key feature of asthma, the characteristics of airway inflammation in children with acute severe asthma are not well defined. The aim of this study was to describe the characteristics of airway inflammation in children with an acute exacerbation of asthma using sputum cell counts and fluid-phase measurements and to examine the changes in these parameters upon resolution of the exacerbation. Children (n = 38) presenting to the Emergency Department with acute asthma underwent successful sputum induction using ultrasonically nebulized normal saline (n = 22), or expectorated sputum spontaneously (n = 16). Sputum induction was repeated at least 2 wk later when the children had recovered (n = 28). Sputum portions were selected, dispersed and total and differential cell counts performed. Neutrophil elastase and EG2-positive eosinophils were assessed and fluid-phase eosinophil cationic protein (ECP), myeloperoxidase (MPO), interleukin-8 (IL-8), and IL-5 were measured. During the acute exacerbation the median (range) total cell count was 8.4 x 106/ml (0.5 to 190.3), and fell significantly at resolution to 1.3 x 106/ml (p < 0.01). The inflammatory cell infiltrate was mixed and included eosinophils (0.8 x 106/ml), neutrophils (3.3 x 106/ml), and mast cells. EG2+cells were high and correlated with the degree of airflow obstruction (r = -0.5, p = 0.02). They decreased significantly at resolution as did supernatant ECP (1,078 versus 272 ng/ml), suggesting that eosinophils were activated during the exacerbation. MPO was 220 ng/ml at exacerbation and fell significantly to 1 ng/ml at resolution. Levels of IL-8 and IL-5 were elevated during the acute exacerbation and IL-8 concentrations decreased at resolution. In conclusion, airway inflammation can be studied in children with acute asthma by sputum induction. Airway inflammation is present during an acute exacerbation of asthma, and is characterized by infiltration and activation of both eosinophils and neutrophils. The heterogeneity of airway inflammation in acute asthma may influence response to corticosteroid therapy.
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Chin, C. D. et al. Microfluidics-based diagnostics of infectious diseases in the developing world. Nat. Med. 17, 1015–1019 (2011).
Yetisen, A. K., Martinez-Hurtado, J. L., Garcia-Melendrez, A., da Cruz Vasconcellos, F. & Lowe, C. R. A smartphone algorithm with inter-phone repeatability for the analysis of colorimetric tests. Sens. Actuators, B 196, 156–160 (2014).
I looked again through my comment to you and I really do not think I psychoanalysed you, although I am sorry if you felt offended by me. I am a psychotherapist but am not a psychoanalyst, so do not analyse people. I did ask you what you were afraid of, because to put your group survival ahead of universal values has to be driven by fear. What else is there?
Beyond the role of immune activation, low CD4 T cell counts, and high viral loads as drivers of neutralizing Ab breadth, recent data suggest that individuals who generate bNAbs have autoimmune-like transcriptional signatures (54–56). These transcriptional programs may enable B cells to break the necessary tolerance to evolve polyreactive B cell receptors and drive extensive affinity maturation (5, 56, 57), even within framework regions that are rarely targeted for somatic mutation in healthy B cells (10). Similarly, IC levels and signaling have been linked to autoimmune signatures in B cells in individuals with rheumatoid arthritis and lupus (58–60). However, whether neutralizers have autoimmune-like signatures due to intrinsic differences in their B cell populations or due to the higher abundance of ICs that can interact with FcRs and CRs is unknown. Nevertheless, it is plausible that increased IC signaling could lead not only to enhanced antigen deposition but also to increased B cell activation, enabling antigen-specific B cells to undergo more extensive maturation, tolerate more mutations, and even develop responses to cross-reactive epitopes. Thus, linked to emerging rationally designed antigens, immunization strategies that also selectively direct the Fc domain of the induced humoral immune response may stimulate the needed maturation to induce protective immunity.
A deleterious effect of ROS on mitochondria is also displayed in a model of age-related skeletal muscle dysfunction. Umanskaya et al demonstrated a decrease in the pathologic intracellular Ca leak with antioxidant treatment. This intracellular finding was associated with gross changes in anatomical function in the form of whole organism exercise capacity and the specific force performance of skeletal muscle47. These findings further strengthen the position that ROS are involved in multiple pathophysiologic processes and the potential for antioxidant treatments that provide a selective yet adequate effect.
Shared decision making is needed for men considering screening to make a decision consistent with their individual values and preferences. However, clinicians need not feel obligated to systematically raise the issue of PSA screening with their patients
Copyright © 2016 by the American Thoracic Society. Asthma in the elderly (.65 yr old) is common and associated with higher morbidity and mortality than asthma in younger patients…. [more]
Kim, J. S. et al. Antitumor effect of skin of Venenum Bufonis in a NCI-H460 tumor regression model. J Acupunct Meridian Stud. 3, 181–187 (2010).
Under lead author Joshua Roth, PhD, who is also affiliated with the Fred Hutchinson Cancer Research Center, the team used a microsimulation model of prostate cancer that links disease progression with individual PSA growth.
Might I suggest , they try behaving the way citizens of a real democracy are required to . Ie , start treating their fellow Israeli “Arab ” citizens , (Palestinians) as human beings .Get used to the normality of everyday life in a real democracy before jumping in head first and suffering the realization of no longer being privileged.
Does a PSA Test Really Matter? â Precision Vaccinations | Calprotectin Elisa Kit Related Video:
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