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Background Although increased circulating levels of malondialdehyde-modified low-density lipoprotein (MDA-LDL) are associated with coronary artery disease (CAD), there is no direct evidence that increased MDA-LDL is a prognostic factor for CAD. Methods Forty-two patients (20 diabetic and 22 non-diabetic patients) who underwent percutaneous coronary intervention (PCI) were enrolled, and their baseline MDA-LDL levels were determined by immunoassay. Follow-up coronary angiography was performed at 2 to 7 months post-PCI. The patients were then divided into 2 groups, with in-stent restenosis (ISR) (n = 13) and without ISR (n = 29), and the baseline MDA-LDL levels were compared. We also studied 34 diabetics with CAD for up to 57 months until the onset of the next coronary event. Results In the diabetic patients, the mean MDA-LDL level was significantly higher in those with ISR than in those without ISR (151 +/− 61 vs. 90 +/− 26 U/l, p = 0.010). A baseline MDA-LDL value of 110 U/l for differentiating between diabetics with and without ISR was defined as the cut-off value. Kaplan–Meier analysis demonstrated that a circulating MDA-LDL of ≥ 110 U/l correlated significantly with a higher prevalence of cardiac events than MDA-LDL Conclusions Circulating MDA-LDL is a useful prognostic marker for future cardiac event in diabetic patients with CAD.

Direct numerical simulation was performed for the spatially advancing turbulent flow and heat transfer in a two-dimensional curved channel equating the radius ratio to 0.92 or 0.8. The frictional Reynolds number was fixed at 150, whereas the Prandtl number was set at 0.71. According to the numerical result, the remarkable enhancement of heat transfer occurred on the outer wall, suggesting the organized vortex activated the heat transfer. The budgets of Reynolds stresses clarified that the onset and growth of the organized flow was assisted by the direct energy transfer from the mean flow.

Familial combined hyperlipidemia (FCHL) is characterized by elevated levels of serum total cholesterol (TC), triglyceride (TG), or both. The increased incidence of coronary artery diseases (CAD) in the patients with FCHL is believed to be caused by circulating atherogenic lipoproteins associated with the complex phenotype. Recent establishment of sensitive detection system for malondialdehyde-modified (MDA)-LDL, which is one of oxidized lipoproteins, showed its increased circulating level in the patients with CAD. In order to know the atherogenic lipoproteins resulted from the dyslipidemia observed in FCHL, we measured the serum MDA-LDL level in the patients. The circulating MDA-LDL level and the ratio of MDA-LDL and LDL-C in FCHL were significantly higher (P

Postprandial hyperlipidemia is frequently accompanied with intra-abdominal visceral accumulation in human subjects. We have found that the decreased lipoprotein lipase (LPL) mass and activity is negatively associated with the amount of visceral fat accumulation. Here, we studied the postprandial hyperlipidemia using the OLETF rat, a model with visceral obesity, in order to clarify the molecular mechanism causing postprandial hyperlipidemia accompanied with visceral obesity. At the same age of 32 weeks, the OLETF rats showed obviously higher plasma leptin, total cholesterol, triglyceride, and HDL-cholesterol levels than the control LETO rats, although the plasma glucose level was not significantly different. Fat-loading test revealed the delayed metabolism of exogenous fat in the OLETF rats compared to the LETO rats, similar to human subjects with visceral obesity. In the obese rats, plasma levels of LPL mass and activities were 60 and 49% of control rats. The expression of LPL gene was decreased in subcutaneous adipose tissues and skeletal muscle of OLETF rats to 40 and 52% compared to those of LETO rats. In OLETF rats, plasma tumor necrosis factor-alpha (TNF-alpha) and insulin levels were increased to 2.0- and 2.3-folds compared to those in control rats. Furthermore, plasma insulin and TNF-alpha levels in OLETF rats were negatively correlated with the expression levels of LPL gene in subcutaneous fat and muscle. These results indicate that decreased LPL mass and activity in the animal model with visceral obesity is possibly caused by decreased expression of LPL gene in tissues mediated by the increased levels of insulin and TNF-alpha. The different expression of LPL gene in tissues associated with the increased levels of insulin and TNF-alpha possibly elucidate the underlying mechanisms involving the postprandial hyperlipidemia observed in visceral obesity.

Direct numerical simulation was performed for the spatially advancing turbulent flow in a two-dimensional curved channel. The fully developed turbulence was introduced into the curved channel through a straight part, and observation was made for how the near-wall turbulence advanced along curved walls. The frictional Reynolds number, Reτ0, was fixed at 150, whereas the radius ratio of the curved channel, α, was changed at three steps; 0.8, 0.92, and 0.975. Five computational tests were performed, which include simulations with changing the spanwise length of the channel or the grid arrangement. The maximum number of grid points was 43,610,112 (=936 × 91 × 512) used in the case of α = 0.92. Numerical results for the curved flow were nearly free from the grid arrangement or the spanwise length of the channel, and changes of the mean velocity qualitatively agreed with the experiment by Kobayashi et al. [Trans. Jpn. Soc. Mech. Eng., Ser. B 57, 4064 (1991)], which both supported credibility of the simulation. ...