21 research outputs found

    International severe asthma registry (ISAR): protocol for a global registry

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    Background: Severe asthma exerts a disproportionately heavy burden on patients and health care. Due to the heterogeneity of the severe asthma population, many patients need to be evaluated to understand the clinical features and outcomes of severe asthma in order to facilitate personalised and targeted care. The International Severe Asthma Registry (ISAR) is a multi-country registry project initiated to aid in this endeavour. Methods: ISAR is a multi-disciplinary initiative benefitting from the combined experience of the ISAR Steering Committee (ISC; comprising 47 clinicians and researchers across 29 countries, who have a special interest and/or experience in severe asthma management or establishment and maintenance of severe asthma registries) in collaboration with scientists and experts in database management and communication. Patients (≥18 years old) receiving treatment according to the 2018 definitions of the Global Initiative for Asthma (GINA) Step 5 or uncontrolled on GINA Step 4 treatment will be included. Data will be collected on a core set of 95 variables identified using the Delphi method. Participating registries will agree to provide access to and share standardised anonymous patient-level data with ISAR. ISAR is a registered data source on the European Network of Centres for Pharmacoepidemiology and Pharmacovigilance. ISAR's collaborators include Optimum Patient Care, the Respiratory Effectiveness Group (REG) and AstraZeneca. ISAR is overseen by the ISC, REG, the Anonymised Data Ethics & Protocol Transparency Committee and the ISAR operational committee, ensuring the conduct of ethical, clinically relevant research that brings value to all key stakeholders. Conclusions: ISAR aims to offer a rich source of real-life data for scientific research to understand and improve disease burden, treatment patterns and patient outcomes in severe asthma. Furthermore, the registry will provide an international platform for research collaboration in respiratory medicine, with the overarching aim of improving primary and secondary care of adults with severe asthma globally.</p

    E-Cigarette Affects the Metabolome of Primary Normal Human Bronchial Epithelial Cells

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    <div><p>E-cigarettes are widely believed to be safer than conventional cigarettes and have been even suggested as aids for smoking cessation. However, while reasonable with some regards, this judgment is not yet supported by adequate biomedical research data. Since bronchial epithelial cells are the immediate target of inhaled toxicants, we hypothesized that exposure to e-cigarettes may affect the metabolome of human bronchial epithelial cells (HBEC) and that the changes are, at least in part, induced by oxidant-driven mechanisms. Therefore, we evaluated the effect of e-cigarette liquid (ECL) on the metabolome of HBEC and examined the potency of antioxidants to protect the cells. We assessed the changes of the intracellular metabolome upon treatment with ECL in comparison of the effect of cigarette smoke condensate (CSC) with mass spectrometry and principal component analysis on air-liquid interface model of normal HBEC. Thereafter, we evaluated the capability of the novel antioxidant tetrapeptide O-methyl-l-tyrosinyl-γ-l-glutamyl-l-cysteinylglycine (UPF1) to attenuate the effect of ECL. ECL caused a significant shift in the metabolome that gradually gained its maximum by the 5<sup>th</sup> hour and receded by the 7<sup>th</sup> hour. A second alteration followed at the 13<sup>th</sup> hour. Treatment with CSC caused a significant initial shift already by the 1<sup>st</sup> hour. ECL, but not CSC, significantly increased the concentrations of arginine, histidine, and xanthine. ECL, in parallel with CSC, increased the content of adenosine diphosphate and decreased that of three lipid species from the phosphatidylcholine family. UPF1 partially counteracted the ECL-induced deviations, UPF1’s maximum effect occurred at the 5<sup>th</sup> hour. The data support our hypothesis that ECL profoundly alters the metabolome of HBEC in a manner, which is comparable and partially overlapping with the effect of CSC. Hence, our results do not support the concept of harmlessness of e-cigarettes.</p></div

    Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor-7

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    F-β(E) for 48 h. B: Increased expression of Tn was detected by Western blot analysis in cell lysates after stimulation with TGF-β(B) for 48 h. The data were quantified by densitometry and are expressed as fold increases above non-stimulated cells (mean ± SEM) (n = 12). D: Augmented expression of Tn protein was detected by flow cytometry in response to LTDcombined with TGF-β, compared with the effect of LTDalone. Difference from isotype control mean fluorescence intensity (MFI) is presented (mean ± SEM). Presence of 5 mM L-cysteine in the culture media did not affect the expression levels of Tn (D, E). *p < 0.05, **p < 0.01, and ***p < 0.001 vs. non-stimulated cells. NS – non-significant.<p><b>Copyright information:</b></p><p>Taken from "Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor"</p><p>http://respiratory-research.com/content/9/1/44</p><p>Respiratory Research 2008;9(1):44-44.</p><p>Published online 26 May 2008</p><p>PMCID:PMC2412865.</p><p></p

    Characteristics of the individuals involved in the measurement of poly(ADP-ribose) polymerase (PARP)-1 mRNA expression in peripheral blood mononuclear cells.

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    <p>Data are presented as mean ± SEM or n (%). <sup>*</sup>To test the equality of the data across the study groups, Kruskal-Wallis test and Pearson’s chi-square test was applied for numeric and nominal variables, respectively; in case of smoking-related variables, non-smoking controls were omitted from the analysis.</p

    Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor-5

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    BAY u9773. There was no statistical difference between the inhibitory effects of MLK and BAY u9773. Data are expressed as mean ± SEM (n = 12) *p < 0.05, **p < 0.01, and ***p < 0.001.<p><b>Copyright information:</b></p><p>Taken from "Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor"</p><p>http://respiratory-research.com/content/9/1/44</p><p>Respiratory Research 2008;9(1):44-44.</p><p>Published online 26 May 2008</p><p>PMCID:PMC2412865.</p><p></p

    Mass spectrum of primary normal human bronchial epithelial cells cultivated in air-liquid interface after exposure to e-cigarette liquid (ECL) (100 μM by nicotine) and 10 μg/mL cigarette smoke condensate (CSC) consisting of 1,822 distinct mass-to-charge signals.

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    <p>The figure represents the proportions of the spectrum that were significantly (p<i><</i>0.05) affected by addition of ECL (392 signals) or CSC (569 signals) during the first 7 h. There were 138 signals that were significantly affected by both stimuli.</p

    Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor-1

    No full text
    F-β(E) for 48 h. B: Increased expression of Tn was detected by Western blot analysis in cell lysates after stimulation with TGF-β(B) for 48 h. The data were quantified by densitometry and are expressed as fold increases above non-stimulated cells (mean ± SEM) (n = 12). D: Augmented expression of Tn protein was detected by flow cytometry in response to LTDcombined with TGF-β, compared with the effect of LTDalone. Difference from isotype control mean fluorescence intensity (MFI) is presented (mean ± SEM). Presence of 5 mM L-cysteine in the culture media did not affect the expression levels of Tn (D, E). *p < 0.05, **p < 0.01, and ***p < 0.001 vs. non-stimulated cells. NS – non-significant.<p><b>Copyright information:</b></p><p>Taken from "Synthesis of tenascin and laminin beta2 chain in human bronchial epithelial cells is enhanced by cysteinyl leukotrienes via CysLTreceptor"</p><p>http://respiratory-research.com/content/9/1/44</p><p>Respiratory Research 2008;9(1):44-44.</p><p>Published online 26 May 2008</p><p>PMCID:PMC2412865.</p><p></p
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