1. HDL in risk prediction and its direct and indirect involvement in atherogenesis 
Paul Durrington 
Atherosclerosis Supplements 
Volume 3, Issue 4, Pages 3-12 (December 2002)
DOI: /S (02)

2. Fig. 1
The risk of CHD as a function of HDL cholesterol total serum cholesterol and LDL cholesterol in 60-year old men whose blood pressure is 140/85 mmHg, who are non-diabetic, non-smokers and whose serum triglyceride concentration is 1.1 mmol/l. For the serum cholesterol and LDL cholesterol curves HDL cholesterol was 1.4 mmol/l and for the HDL cholesterol curve serum cholesterol was 6.0 mmol/l. Calculation based on equations in [34].
Atherosclerosis Supplements 2002 3, 3-12DOI: ( /S (02) )

3. Fig. 2
Mean (S.E.) serum HDL cholesterol concentration in men and women according to the number of CHD risk factors they possess [27].
Atherosclerosis Supplements 2002 3, 3-12DOI: ( /S (02) )

4. Fig. 3
HDL metabolism. CE stored within cells can be mobilised by activation of CE hydrolase stimulated by binding of HDL at the cell surface. The FC thus liberated can leave the cell via the ATP binding cassette A1 (ABCA1) to be taken up by preβHDL where it is esterified by LCAT converting the particle to HDL3 and then HDL2. Thence it can be taken up by the liver or be transferred to apo B-containing lipoproteins by cholesteryl ester transfer protein (CETP). From these it may be transported back to the liver or re-enter the tissues for example via the LDL receptor (LDLR). The action of CETP on LDL may also contribute to the formation of small, dense LDL. The pathways which contribute to reverse cholesterol transport are indicated by broken lines. Binding of HDL to receptors, such as the scavenger receptor B1 (SRB1) in the tissues in man probably does not lead to tissue cholesterol uptake, but to an intracellular signalling process activating CE hydrolase. In the liver, it probably does allow the removal of CE from HDL without degradation of the HDL particle which is re-released into the circulation. Additional abbreviations: LDL receptor-like protein (LRP), non-receptor mediated uptake (NMRU).
Atherosclerosis Supplements 2002 3, 3-12DOI: ( /S (02) )

5. Fig. 4
The effect of incubating fasting serum at 37°C (a) on the CE concentration in serum, HDL and apo B-containing lipoproteins (VLDL/LDL) in the presence of an LCAT inhibitor, 5,5-dithio-bis(2-nitrobenzoic acid) (DTNB) and (b) on the serum triglyceride concentration in serum, HDL and apo B-containing lipoproteins (VLDL/LDL) without DTNB. The exchange of CE and triglycerides between HDL and the apo B-containing lipoproteins is clearly evident. Without DTNB there is an increase in total CE due to esterification of FC by LCAT on HDL which tends to maintain the level of CE on HDL constant whilst that transferred to apo B-containing lipoprotein is even greater [50].
Atherosclerosis Supplements 2002 3, 3-12DOI: ( /S (02) )

6. Fig. 5
The effect on the concentration of preβHDL of incubating fasting serum at 37°C in the presence and absence of DTNB [66].
Atherosclerosis Supplements 2002 3, 3-12DOI: ( /S (02) )