Candidate genetic variations after filtering in all samples with controls.

<p>UTR =  untranslated region, SNV =  single nucleotide variation, DIV =  deletion/insertion variation, chr = chromosome, array =  capture array, spl site =  splice site, prom = promoter.</p

Per base coverage of known candidate genes in oligodendrogliomas located on 1p or 19q.

<p>Min/Max: lowest/highest coverage, % covered: the percentage of bases sequenced at least 7 times (the cutoff used for our analysis).</p

Coverage plot of all samples.

<p>Depicted is the percentage of targeted bases (y-axis) that is covered at least n times (x-axis) per sample.</p

Percentage methylation of two different CpG sites (cg24919884 and cg02737335) within the ARHGEF16 locus.

<p>Values correspond to the fraction of methylation (scale 0–1).</p

Patient characteristics of all tumor samples.

<p>OD  =  oligodendroglioma, OA  =  oligoastrocytoma, KPS  =  Karnofsky performance score,</p><p>PCV  =  procarbazine, lomustine, vincristine.</p><p>F =  female, M =  male, OD  =  oligodendroglioma, OA  =  oligoastrocytoma, grades II or III. Age =  age at diagnosis. KPS  =  Karnofsky performance score, PCV  =  procarbazine, lomustine, vincristine. Surgery types: PR =  partial resection, CR =  complete resection, SB =  stereotactic biopsy. RT =  radiotherapy, CT =  Chemotherapy.</p

ARHGEF16 (RefSeq: NM_014448.3) mutation and promoter methylation.

<p>A; Upper lane: part of the sequence of ARHGEF16 with the missense mutation (2125G->A) in tumor sample 8. Lower lane: sequence of the same region of ARHGEF16 in the matching control DNA. B; Kaplan Meier survival curve of oligodendrogliomas (n = 39) and oligoastrocytomas (n = 11) with unmethylated ARHGEF16 (< median) (black line) or methylated ARHGEF16 (> median) (grey line). ** = p<0.01.</p

Deep Proteome Profiling of Circulating Granulocytes Reveals Bactericidal/Permeability-Increasing Protein as a Biomarker for Severe Atherosclerotic Coronary Stenosis

Coronary atherosclerosis represents the major cause of death in Western societies. As atherosclerosis typically progresses over years without giving rise to clinical symptoms, biomarkers are urgently needed to identify patients at risk. Over the past decade, evidence has accumulated suggesting cross-talk between the diseased vasculature and cells of the innate immune system. We therefore employed proteomics to search for biomarkers associated with severe atherosclerotic coronary lumen stenosis in circulating leukocytes. In a two-phase approach, we first performed in-depth quantitative profiling of the granulocyte proteome on a small pooled cohort of patients suffering from chronic (sub)­total coronary occlusion and matched control patients using stable isotope peptide labeling, two-dimensional LC–MS/MS and data-dependent decision tree fragmentation. Over 3000 proteins were quantified, among which 57 candidate biomarker proteins remained after stringent filtering. The most promising biomarker candidates were subsequently verified in the individual samples of the discovery cohort using label-free, single-run LC–MS/MS analysis, as well as in an independent verification cohort of 25 patients with total coronary occlusion (CTO) and 19 matched controls. Our data reveal bactericidal/permeability-increasing protein (BPI) as a promising biomarker for severe atherosclerotic coronary stenosis, being down-regulated in circulating granulocytes of CTO patients

Deep Proteome Profiling of Circulating Granulocytes Reveals Bactericidal/Permeability-Increasing Protein as a Biomarker for Severe Atherosclerotic Coronary Stenosis

Coronary atherosclerosis represents the major cause of death in Western societies. As atherosclerosis typically progresses over years without giving rise to clinical symptoms, biomarkers are urgently needed to identify patients at risk. Over the past decade, evidence has accumulated suggesting cross-talk between the diseased vasculature and cells of the innate immune system. We therefore employed proteomics to search for biomarkers associated with severe atherosclerotic coronary lumen stenosis in circulating leukocytes. In a two-phase approach, we first performed in-depth quantitative profiling of the granulocyte proteome on a small pooled cohort of patients suffering from chronic (sub)­total coronary occlusion and matched control patients using stable isotope peptide labeling, two-dimensional LC–MS/MS and data-dependent decision tree fragmentation. Over 3000 proteins were quantified, among which 57 candidate biomarker proteins remained after stringent filtering. The most promising biomarker candidates were subsequently verified in the individual samples of the discovery cohort using label-free, single-run LC–MS/MS analysis, as well as in an independent verification cohort of 25 patients with total coronary occlusion (CTO) and 19 matched controls. Our data reveal bactericidal/permeability-increasing protein (BPI) as a promising biomarker for severe atherosclerotic coronary stenosis, being down-regulated in circulating granulocytes of CTO patients

Conversion of dose-response curve into area under the curve.

<p>In order to compare total platelet reactivity between patients, we derived the area under the curve from each dose response curve. MFI = mean fluorescence intensity, AUC = area under curve, ADP = adenosine diphosphate.</p

Baseline characteristics.

<p>Continuous values are expressed as mean ± standard deviation (unless specified otherwise). Categorical values are expressed as number of total (percentage).</p><p>CG = Cockroft-Gault, CEA = carotid endarterectomy, IQR = interquartile range.</p