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Smokers with airflow limitation had exaggerated subclinical atherosclerosis. This study suggests that middle-aged men who are susceptible to COPD may also be susceptible to vascular atherosclerosis by smoking, and atherosclerotic change starts early in the disease process of COPD.

OBJECTIVE -Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) differ in their risk of all-cause and cardiovascular mortality, but previous cross-sectional studies have suggested little difference in their levels of lipids or blood pressure. We compared the white blood cell (WBC) count between subjects with IFG and IGT.RESEARCH DESIGN AND METHODS -The subjects were 4,720 nondiabetic Japanese men aged 24 -84 years. Based on the 75-g oral glucose tolerance test, the subjects were classified into the following four groups: normal fasting glucose/normal glucose tolerance (n ϭ 3,753), isolated IFG (n ϭ 290), isolated IGT (n ϭ 476), and IFG/IGT (n ϭ 201). We compared the WBC count among the four groups and investigated variables that showed a significant association with the WBC count.RESULTS -The isolated IGT group had a significantly higher WBC count than the isolated IFG group (6,530 vs. 6,210/mm 3 , P Ͻ 0.05). By stepwise analyses, age, triglycerides, HDL cholesterol, fasting insulin, and 2-h postchallenge plasma glucose (PG) showed an independent association with the WBC count (adjusted R 2 ϭ 0.057). In the analysis stratified by smoking status, the WBC count was independently associated with 2-h PG and triglycerides, irrespective of smoking status.CONCLUSIONS -Individuals with isolated IGT had a significantly higher WBC count than those with isolated IFG. The WBC count was associated with 2-h PG and various components of the metabolic syndrome.

As a means of estimating the extent of atherosclerosis in large arteries, our results show that both brachial ankle pulse wave velocity and cardio ankle vascular index are useful and that cardio ankle vascular index may have some advantages in its application to patients taking blood pressure-lowering medication because of the minimum effect of blood pressure on its measurement values. The cardio ankle vascular index has increased performance over brachial ankle pulse wave velocity in predicting the coronary artery disease.

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Lipid microemulsion of phospholipid and triglyceride with the size of low-density lipoprotein was capable of removing cholesterol from cholesterol-loaded mouse peritoneal macrophages, resulting in reduction of intracellularly accumulated cholesteryl ester. Apolipoproteins (apo) A-I, A-II, C-III, and E bound to the surface of the microemulsion did not modulate the interaction of the microemulsion with the cells in terms of the cholesterol efflux. The cholesterol removal by the microemulsion was enhanced by some 30% only when apoA-I, -A-II, and -E were present in excess to provide their free forms in the medium, but apoC-III did not show such an effect even by its excess amount. The kinetics including the results with apoC-III were consistent with a model that the apparent enhancement was due to generation of pre-beta high-density lipoprotein (HDL)-like particles upon the interaction of free apolipoproteins with macrophages [Hara, H., & Yokoyama, S. (1991) J. Biol. Chem. 266, 3080-3086]. However, pre beta-HDL-like particle was not detected after 6- and 24-h incubation in the medium where cholesterol efflux to the emulsion was maximally enhanced by the apolipoproteins, and cholesterol and phospholipids removed from the cells were all found with the microemulsions. It was also shown separately that the lipids in pre beta-HDL-like particles generated by apoA-I and macrophages were rapidly, within the order of minutes, transferred to the apo-lipoprotein-covered microemulsions when they were incubated together. Thus, the data were consistent with a model that the free form of certain apolipoproteins, such as apoA-I, -A-II, and -E but not apoC-III, generates pre beta-HDL-like particles with cellular lipids in situ and these particles act as mediators for cholesterol transfer from the cells to other lipoproteins.

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