Maximum circulating concentration of complement components associated with the classical and lectin pathways of activation, C1q, C2 and C4b, and end stage mediators common to all pathways, C5 and C9, were increased in the first seven days after stroke in comparison to non-stroke controls

Maximum circulating concentration of complement components associated with the classical and lectin pathways of activation, C1q, C2 and C4b, and end stage mediators common to all pathways, C5 and C9, were increased in the first seven days after stroke in comparison to non-stroke controls. g/ml) – Physique 5 full data excel format.xlsx (maximum concentrations of noradrenaline in ng/ml) Extended data Edinburgh Data Share: Supplementary Figures: Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence. https://doi.org/10.7488/ds/2626 9 BMS-193885 This project contains the following extended datain the zip folder SupplementaryData: – Supplementary Physique 1.tif (physique showing maximum concentrations of immunoglobulin) – Supplementary Figure 2.tif (physique showing maximum concentrations of complement components C3b/iC3b, C3, C4, Factor H and Properdin) – Supplementary Figure 3.tif (physique showing minimum concentrations of complement components C1q, C5, C9, C2 and C4b) – Supplementary Figure 4.tif (physique showing minimum concentrations of noradrenaline) – Supplementary Table 1.tif (table of baseline characteristics of stroke patients and stratification of groups) – Supplementary Physique 5.tif (physique showing the percentage of patients reaching minimum circulating concentration of immunoglobulin subsets at each sampling time point) – Supplementary Figure 6.tif (physique showing the percentage of patients reaching minimum circulating concentration of BMS-193885 complement components reduced by stroke at each sampling time point) – Supplementary Figure 7.tif (physique showing the percentage BMS-193885 of patients reaching maximum circulating concentration of complement components increased by stroke at each sampling time point) – Supplementary Figure 8.tif (physique showing immunoglobulin concentration in IL-1ra and placebo treated patients at individual sampling points after stroke) – Supplementary Figure 9.tif (physique showing alternative pathway complement BMS-193885 concentration in IL-1ra and placebo treated patients at individual sampling points after stroke) – Supplementary Figure 10.tif (physique showing classical pathway complement concentration in IL-1ra and placebo treated patients at individual sampling points after stroke) – Supplementary Figure 11.tif (physique showing complement concentration in IL-1ra and placebo treated patients at individual sampling points after stroke) – Data Supplementary Fig 1.xlsx – Data Supplementary Fig 4.xlsx (data underlying Supplementary Figures 1-4) – Data Supplementary Fig 5.xlsx (Supplementary Table 1 in spreadsheet format) – Complement time course data Supplementary figures 6, 7, 9, 10, 11.xlsx (data underlying supplementary figures 6, 7, 9 10 and 11) – Immunoglobulin time course data Supplementary figures 5, 8.xlsx (data underlying supplementary figures 5 and 8) Data are available under the terms of the Creative Commons Attribution 4.0 International license (CC-BY 4.0). Version Changes Revised.?Amendments from Version 1 We are pleased the reviewer recognises the relevance of this study to the future treatment of stroke patients and thank them for their insightful and constructive comments. We have completed the suggested reanalysis of our data including determining at which time point maximum and minimum concentrations were reached in individual mediators and repeated measures analysis of samples at individual time points in comparison to admission. As expected, these data demonstrate the high variability in individual patient kinetics and confirm that assessing minimal or maximal concentrations during this short time window (1 week) can enable discovery of early responses to stroke that are biologically meaningful but where peaks/ troughs may be occurring at slightly different time point in individual patients. Importantly, no differences in patient kinetics were apparent in placebo and IL-1ra treated groups further confirming the key findings that IL-1Ra has no significant additional effect on these mediators over and above the effects of stroke. Additionally, we have added the requested information to the manuscript on the lack of Rabbit Polyclonal to NOX1 thrombolytic therapy within this cohort of stroke patients, the use of heparin to collect blood samples and the identification and discussion of the distribution of haemorrhagic versus ischemic stroke patients within each treatment group. Patients who potentially had genetic deficits in MBL production were identified and excluded from analysis and our discussion. Finally, we agree with the reviewer that our method limits the capacity to discuss these findings in terms of activation of complement pathways as we cannot associate these changes to a specific time post stroke or post contamination. We have altered our discussion of the data to remove any speculation about activation or suppression of complement pathways and instead have reported the overall changes in concentration and their relationship to the.

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