1. Subjects with familial hypercholesterolemia are characterized by an inflammatory phenotype despite long-term intensive cholesterol lowering treatment 
Kirsten B. Holven, Ingunn Narverud, Henriette W. Lindvig, Bente Halvorsen, Gisle Langslet, Marit S. Nenseter, Stine M. Ulven, Leiv Ose, Pål Aukrust, Kjetil Retterstøl 
Atherosclerosis 
Volume 233, Issue 2, Pages (April 2014)
DOI: /j.atherosclerosis
Copyright © 2014 Elsevier Ireland Ltd Terms and Conditions

2. Fig. 1
PBMC gene expression of CD137 (A), CD137L (B), LIGHT (C) HVEM (LIGHT receptor) (D), CD40 (E), CD40L (F), TNFR1 (G), TNFR2 (H) and TNFα (I) in FH subjects (n = 33; n = 32 for TNFR1) and healthy subjects (n = 10). The horizontal bars represent median values.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2014 Elsevier Ireland Ltd Terms and Conditions

3. Fig. 2
PBMC gene expression of OX40 (A), OX40L (B), TRAIL (C) TRAIL Receptor R1 (D), RANK (E), RANKL (F), BAFF (G) and BAFFR (H) in FH subjects (n = 33) and healthy subjects (n = 10; n = 9 for OX40, OX40L, TRAIL, TRAIL R1, RANK and RANKL). The horizontal bars represent median values.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2014 Elsevier Ireland Ltd Terms and Conditions

4. Fig. 3
Panel A shows the release of TNFα in PBMC isolated from FH subjects (n = 32l) and healthy controls (n = 7 for LPS and n = 8 for isoproterenol) after 24 h in the presence of LPS (1 ng/ml) or the β-adrenergic receptor agonist isoproterenol (50 μg/ml) in combination with autologous serum (5%). Panel B shows the effect of serum on spontaneous release of TNFα from PBMCs isolated from healthy control subjects (Ctr; n = 9) and FH subjects (FH; n = 32). The cells were incubated in the presence of heat-inactivated serum from a FH patient (FH-serum) or a control subject (Ctr-serum). Data are presented as mean (SEM).* P < 0.05 vs unstimulated (unstim.) cells.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2014 Elsevier Ireland Ltd Terms and Conditions