Arginine, ADMA and SDMA plasma levels.

<p>Arginine (panel A), asymmetric dimethylarginine (ADMA; panel B), and symmetric dimethylarginine (SDMA; panel C) plasma levels (mean±SD values) in healthy subjects (n = 20), in controls with chronic kidney disease (CKD; n = 10), and in NSTEMI patients without (n = 71) and with (n = 33) CKD.</p

Baseline characteristics of the study patients.

*<p>By Fisher exact test.</p>§<p>by Wilcoxon Rank Sum Test.</p><p>ACE = angiotensin-converting enzyme; ARB = angiotensin II receptor blocker; CABG = coronary artery bypass graft surgery; CKD = chronic kidney disease; CRP = C-reactive protein; eGFR = estimated glomerular filtration rate; NA = not applicable; PCI = percutaneous coronary intervention.</p

Relationships between NO synthesis inhibitors and renal function.

<p>Relationship between asymmetric (ADMA; upper panel) and symmetric (SDMA; lower panel) dimethylarginine plasma levels and estimated glomerular filtration rate (eGFR) in the study population.</p

Cox regression analysis for the primary end point of the study (composite outcome of cardiac death and myocardial infarction).

<p>Hazard ratios (HR) in models 1–4 are adjusted for age, hemoglobin and left ventricular ejection fraction; HRs in models 5–7 are also mutually adjusted.</p><p>HRs for CKD are vs. no-CKD; for all other variables, HRs are for values above vs. below median.</p><p>ADMA = asymmetric dimethylarginine; CKD = chronic kidney disease; CI = confidence intervals; SDMA = symmetric dimethylarginine.</p

Kaplan-Meier survival analyses during follow-up.

<p>Composite outcomes of cardiac death and myocardial infarction according to concentrations of plasma arginine (panel A), asymmetric dimethylarginine (ADMA; panel B), and symmetric dimethylarginine (SDMA; panel C), divided by median levels. P values by log-rank test are shown.</p

Effects of HDL isolated from carriers of CETP mutations and controls on VCAM-1 expression in TNFα-stimulated HUVEC.

<p>Cells were incubated overnight with HDL, HDL2, or HDL3 isolated from 7 heterozygous carriers of CETP mutations and age-sex matched controls (n = 8), at the concentration of 1.0 mg of protein/ml, before stimulation with TNFα for 8 hours. Results are expressed as percentage of VCAM-1 concentration in conditioned media of untreated TNFα-stimulated cells. Data points for each study participant are shown.</p

Effect of apoE depletion on eNOS expression in HUVEC.

<p>Panel A. HDL2 isolated from the homozygous carrier of the R37X CETP mutation were separated by 2D electrophoresis, followed by anti apoA-I or anti apoE immunodetection, before (−) and after (+) incubation with heparin-MnCl₂. Panel B. Cells were incubated overnight with HDL2 (1 mg/ml) from the homozygous carrier of the R37X CETP mutation and from controls (n = 3) before (full bars) and after (open bars) treatment with heparin-MnCl₂. Western blot analysis of eNOS protein was performed, and eNOS protein band intensities were normalized for β-actin values and expressed as fold of increase in treated vs. untreated.</p

GGE analysis of purified HDL2 and HDL3.

<p>HDL fractions isolated from the homozygote, and a representative heterozygote and control were analyzed by GGE.</p

2D electrophoresis analysis of purified HDL.

<p>HDL isolated from the homozygote, and a representative heterozygote and control were separated by 2D electrophoresis and immunodetected with anti apoA-I and anti apoE antibodies.</p

Sphingosine-1-phosphate levels in HDL, HDL2, and HDL3.

<p>Data are expressed as mean±SD.</p