536 research outputs found

    Human interleukin-13 activates the interleukin-4-dependent transcription factor NF-IL4 sharing a DNA binding motif with an interferon-γ-induced nuclear binding factor

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    AbstractThe effects of interleukin-13 (IL-13) and interleukin-4 (IL-4) on cellular functions were shown to be quite similar. We provide evidence that in monocytes as well as in T lymphocytes both IL-4 and IL- 13 activate the same recently identified transcription factor NF-IL4 which binds to the specific responsive element IL-4RE. In addition, we show that a nuclear factor activated by interferon-γ also interacts with the IL-4RE. It differs from NF-IL4 in the electrophoretic mobility of the complex with DNA, in its DNA-binding specificity and in the proteins interacting with the DNA sequence. Sensitivity against various enzyme inhibitors suggests that components of the signal transduction pathway are shared by all three cytokines

    Cloning of Salmonella enterica serovar Enteritidis fimbrial protein SefA as a surface protein in Escherichia coli confers the ability to attach to eukaryotic cell lines

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    The gene for the Salmonella enterica serovar Enteritidis fimbrial protein SefA was cloned into an Escherichia coli surface expression vector and confirmed by Western blot assay. E. coli clones expressing SefA attached to avian ovary granulosa cells and HEp-2 cells, providing evidence for the involvement of SefA in the ability of Salmonella to attach to eukaryotic cells.Peer reviewedAnimal Scienc

    Biomarkers of Clot Activation and Degradation and Risk of Future Major Cardiovascular Events in Acute Exacerbation of COPD: A Cohort Sub-Study in a Randomized Trial Population

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    COPD exacerbation; Coagulation; Cross-linked fibrin degradationExacerbación de la EPOC; Coagulación; Degradación de fibrina reticuladaExacerbació de la MPOC; Coagulació; Degradació de fibrina reticuladaCardiovascular diseases are common in patients with chronic obstructive pulmonary disease (COPD). Clot formation and resolution secondary to systemic inflammation may be a part of the explanation. The aim was to determine whether biomarkers of clot formation (products of von Willebrand Factor formation and activation) and clot resolution (product of fibrin degeneration) during COPD exacerbation predicted major cardiovascular events (MACE). The cohort was based on clinical data and biobank plasma samples from a trial including patients admitted with an acute exacerbation of COPD (CORTICO-COP). Neo-epitope biomarkers of formation and the activation of von Willebrand factor (VWF-N and V-WFA, respectively) and cross-linked fibrin degradation (X-FIB) were assessed using ELISAs in EDTA plasma at the time of acute admission, and analyzed for time-to-first MACE within 36 months, using multivariable Cox proportional hazards models. In total, 299/318 participants had samples available for analysis. The risk of MACE for patients in the upper quartile of each biomarker versus the lower quartile was: X-FIB: HR 0.98 (95% CI 0.65–1.48), VWF-N: HR 1.56 (95% CI 1.07–2.27), and VWF-A: HR 0.78 (95% CI 0.52–1.16). Thus, in COPD patients with an acute exacerbation, VWF-N was associated with future MACE and warrants further studies in a larger population.This study was funded by the Danish Regions Medical Fund (grant no. 5894/16), the Danish Council for Independent Research (grant no. 6110-00268B), and the Novo Nordisk foundation (grant no. NNF20OC0060657). Author D.D.M. received personal funding from the Danish National Research Foundation (DNRF126)

    Multicentre Performance Evaluation of the Elecsys Anti-SARS-CoV-2 Immunoassay as an Aid in Determining Previous Exposure to SARS-CoV-2

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    Introduction We performed a multicentre evaluation of the Elecsys® Anti-SARS-CoV-2 immunoassay (Roche Diagnostics), an assay utilising a recombinant protein representing the nucleocapsid (N) antigen, for the in vitro qualitative detection of antibodies to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Methods Specificity was evaluated using serum/plasma samples from blood donors and routine diagnostic specimens collected before September 2019 (i.e., presumed negative for SARS-CoV-2-specific antibodies); sensitivity was evaluated using samples from patients with polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection. Point estimates and 95% confidence intervals (CIs) were calculated. Method comparison was performed versus commercially available assays. Results Overall specificity for the Elecsys Anti-SARS-CoV-2 immunoassay (n = 9575) was 99.85% (95% CI 99.75–99.92): blood donors (n = 6714; 99.82%), routine diagnostic specimens (n = 2861; 99.93%), pregnant women (n = 2256; 99.91%), paediatric samples (n = 205; 100.00%). The Elecsys Anti-SARS-CoV-2 immunoassay demonstrated significantly higher specificity versus LIAISON SARS-CoV-2 S1/S2 IgG (99.71% vs. 98.48%), EUROIMMUN Anti-SARS-CoV-2 IgG (100.00% vs. 94.87%), ADVIA Centaur SARS-CoV-2 Total (100.00% vs. 87.32%) and iFlash SARS-CoV-2 IgM (100.00% vs. 99.58%) assays, and comparable specificity to ARCHITECT SARS-CoV-2 IgG (99.75% vs. 99.65%) and iFlash SARS-CoV-2 IgG (100.00% vs. 100.00%) assays. Overall sensitivity for Elecsys Anti-SARS-CoV-2 immunoassay samples drawn at least 14 days post-PCR confirmation (n = 219) was 93.61% (95% CI 89.51–96.46). No statistically significant differences in sensitivity were observed between the Elecsys Anti-SARS-CoV-2 immunoassay versus EUROIMMUN Anti-SARS-CoV-2 IgG (90.32% vs. 95.16%) and ARCHITECT SARS-CoV-2 IgG (84.81% vs. 87.34%) assays. The Elecsys Anti-SARS-CoV-2 immunoassay showed significantly lower sensitivity versus ADVIA Centaur SARS-CoV-2 Total (85.19% vs. 95.06%) and iFlash SARS-CoV-2 IgG (86.25% vs. 93.75%) assays, but significantly higher sensitivity versus the iFlash SARS-CoV-2 IgM assay (86.25% vs. 33.75%). Conclusion The Elecsys Anti-SARS-CoV-2 immunoassay demonstrated very high specificity and high sensitivity in samples collected at least 14 days post-PCR confirmation of SARS-CoV-2 infection, supporting its use to aid in determination of previous exposure to SARS-CoV-2
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