Post-hoc correlation between serum lycopene concentrations and EDV.

<p>Relationship between absolute change in serum lycopene concentrations and absolute change in endothelial dependent vasodilatation (EDV; forearm blood flow response to 15 µg/min acetylcholine measured as %change from preceding saline baseline) for all trial subjects. Absolute change in serum lycopene calculated as final visit serum lycopene minus baseline serum lycopene. Absolute change in EDV calculated as final visit EDV minus baseline EDV. r: correlation coefficient calculated using Pearson correlation analysis.</p

Baseline Demographics of CVD Patients and HV arms.

<p>Data are presented as mean (standard deviation - SD) or numbers (%). ACE-I: Angiotensin Converting Enzyme Inhibitor; ARB: Angiotensin Receptor Blocker; CVD: cardiovascular disease; EtOH: Alcohol; HV: healthy volunteer.</p

Post-hoc comparisons of baseline values between CVD Patients and HV arms.

<p>Data are presented as mean values (standard deviation - SD). *<i>P</i>-value is for comparison between cardiovascular disease (CVD) patients arm and healthy volunteer (HV) arm at baseline using unpaired, 2-tailed Student <i>t</i>-tests. AIx – augmentation index; DBP – diastolic blood pressure; HDL – high-density lipoprotein; hsCRP – high sensitivity C-reactive protein; LDL – low-density lipoprotein; ox-LDL – oxidised low-density lipoprotein, PWV – pulse wave velocity; SBP – systolic blood pressure.</p

Vascular and Laboratory Assessments in CVD Patients Arm.

<p>Data are presented as mean values (standard error - SE). *<i>P</i>-value is for overall comparison in delta (day 56 - day 1) values across placebo and lycopene treated groups. AIx – augmentation index; CVD: cardiovascular disease; DBP – diastolic blood pressure; HDL – high-density lipoprotein; hsCRP – high sensitivity C-reactive protein; IL – interleukin; LDL – low-density lipoprotein; MMP-9– matrix metalloproteinase; ox-LDL – oxidised low-density lipoprotein, PWV – pulse wave velocity; SBP – systolic blood pressure; TNF – tumour necrosis factor.</p

Schematic of forearm blood flow protocol.

<p>ACh: Acetylcholine; SNP: Sodium Nitroprusside; L-NMMA: N^G-monomethyl-L-arginine; H: Haemodynamic measurements.</p

Flow diagram of subjects through the study.

<p>The safety population consisted of anyone who received at least 1*Reasons for failure to enrol included not meeting inclusion criteria, an inability to attend laboratory for assessments within the appropriate timeframe, patient withdrawal, inability to lie flat for a period of time for the studies, or an inability to cannulate the brachial artery. **Quality control evaluation done by two independent parties. Reasons for non-evaluable data and consequent exclusion from final forearm blood flow (FBF) analysis (before unblinding and statistical analysis) included incomplete data sets, non-evaluable sets, and FBF procedure variation.</p

Additional file 1: of Vascular inflammation and aortic stiffness: potential mechanisms of increased vascular risk in chronic obstructive pulmonary disease

Scan Image Protocols. (DOCX 92 kb

Additional file 1: of Quantitative analysis of dynamic 18F-FDG PET/CT for measurement of lung inflammation

Supplemental data for quantitative analysis of dynamic 18F-FDG PET/CT for measurement of lung inflammation. (DOCX 318 kb

The p38 mitogen activated protein kinase inhibitor losmapimod in chronic obstructive pulmonary disease patients with systemic inflammation, stratified by fibrinogen: A randomised double-blind placebo-controlled trial

<div><p>Background</p><p>Cardiovascular disease is a major cause of morbidity and mortality in COPD patients. Systemic inflammation associated with COPD, is often hypothesised as a causal factor. p38 mitogen-activated protein kinases play a key role in the inflammatory pathogenesis of COPD and atherosclerosis.</p><p>Objectives</p><p>This study sought to evaluate the effects of losmapimod, a p38 mitogen-activated protein kinase (MAPK) inhibitor, on vascular inflammation and endothelial function in chronic obstructive pulmonary disease (COPD) patients with systemic inflammation (defined by plasma fibrinogen >2·8g/l).</p><p>Methods</p><p>This was a randomised, double-blind, placebo-controlled, Phase II trial that recruited COPD patients with plasma fibrinogen >2.8g/l. Participants were randomly assigned by an online program to losmapimod 7·5mg or placebo tablets twice daily for 16 weeks. Pre- and post-dose ¹⁸F-Fluorodeoxyglucose positron emission tomography co-registered with computed tomography (FDG PET/CT) imaging of the aorta and carotid arteries was performed to quantify arterial inflammation, defined by the tissue-to-blood ratio (TBR) from scan images. Endothelial function was assessed by brachial artery flow-mediated dilatation (FMD).</p><p>Results</p><p>We screened 160 patients, of whom, 36 and 37 were randomised to losmapimod or placebo. The treatment effect of losmapimod compared to placebo was not significant, at -0·05 for TBR (95% CI: -0·17, 0·07), p = 0·42, and +0·40% for FMD (95% CI: -1·66, 2·47), p = 0·70. The frequency of adverse events reported was similar in both treatment groups.</p><p>Conclusions</p><p>In this plasma fibrinogen-enriched study, losmapimod had no effect on arterial inflammation and endothelial function at 16 weeks of treatment, although it was well tolerated with no significant safety concerns. These findings do not support the concept that losmapimod is an effective treatment for the adverse cardiovascular manifestations of COPD.</p></div

L'Humanité : früher die Neue Welt : deutschsprachiges Organ der Kommunistischen Partei (SFIC)

28 avril 19251925/04/28 (N98).Appartient à l’ensemble documentaire : Alsace