Dyslipidemia is one of the most important factors for coronary artery disease (CAD). The atherogenic index of plasma (AIP), a new comprehensive lipid index, might be a strong marker for predicting the risk of CAD.A hospital-based case–control study including 2936 CAD patients and 2451 controls was conducted in a Chinese population. Traditional lipid parameters were detected, and nontraditional lipid comprehensive indexes were calculated.Compared with controls, CAD patients had higher levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C). By contrast, the level of high-density lipoprotein cholesterol (HDL-C) was lower in CAD patients. The values of nontraditional lipid profiles, including non-HDL-C, TC/HDL-C, LDL-C/HDL-C, non-HDL-C/HDL-C (atherogenic index, AI), TC∗TG∗LDL/HDL-C (lipoprotein combine index, LCI), and lg (TG/HDL-C) (AIP), were all significantly higher in the cases than in the controls. The results of Pearson correlation analyses indicated that AIP was positively and significantly correlated with TC (r = 0.125, P < .001), TG (r = 0.810, P < .001), LDL-C (r = 0.035, P < .001), non-HDL-C (r = 0.322, P < .001), TC/HDL-C (r = 0.669, P < .001), LDL-C/HDL-C (r = 0.447, P < .001), AI (r = 0.669, P < .001), and LCI (r = 0.688, P < .001) and was negatively correlated with age (r = −0.122, P < .001) and HDL-C (r = −0.632, P < .001). In the univariate logistic regression analysis, AIP was the lipid parameter that was most strongly associated with CAD, with an unadjusted odds ratio of 1.782 (95% confidence interval: 1.490–2.131, P < .001), for an increase of 1-SD. Multivariate logistic regression analyses revealed that AIP was an independent risk factor for CAD.AIP might be a strong and independent predictor for CAD in the Chinese Han population.

Ubiquitin-specific protease 5 (USP5) is a deubiquitinating enzyme that functions as an oncoprotein in a variety of human cancers. However, the expression and role of USP5 in the metastasis of non-small cell lung cancer (NSCLC) have not been addressed. In this study, we examined the expression and prognostic significance of USP5 in NSCLC. The results revealed that USP5 was overexpressed and correlated with metastasis and overall survival in NSCLC tissues. A further in vitro study revealed that the levels of USP5 protein in NSCLC cells were associated with epithelial-mesenchymal transition (EMT) markers. Furthermore, USP5 overexpression significantly enhanced, whereas USP5 silencing significantly decreased the expression of EMT proteins and migration and invasion of NSCLC cells. In addition, the results from western blotting demonstrated that USP5 regulated EMT via the Wnt/b-catenin signaling pathway. Further immunohistochemical analysis revealed that USP5 was significantly associated with the expression of b-catenin and EMT markers in NSCLC tissues. Overall, USP5 upregulation is associated with tumor metastasis and poor prognosis in patients with NSCLC. USP5 promotes EMT and the invasion and migration of NSCLC cells. Therefore, USP5 may serve as a novel prognostic biomarker and provide a potential target for the treatment of metastasis in NSCLC.

Abstract. The aim of the present study was to investigate the cardioprotective effect of tanshinone IIA and the underlying molecular mechanisms. An in vitro model of oxidative stress injury was established in cardiac H9c2 cells, and the effects of tanshinone IIa were investigated using cell viability, reverse transcription-quantitative polymerase chain reaction and western blotting assays. The results demonstrated that tanshinone IIA protects H9c2 cells from H 2 O 2 -induced cell death in a concentration-dependent manner, via a mechanism involving microRNA-133 (miR-133), and that treatment with TIIA alone exerted no cytotoxic effects on H9c2. In order to further elucidate the mechanisms underlying the actions of TIIA, reverse transcription-quantitative polymease chain reaction and western blot analysis were performed. Reductions in miR-133 expression levels induced by increasing concentrations of H 2 O 2 were reversed by treatment with tanshinone IIA. In addition, the inhibition of miR-133 by transfection with an miR-133 inhibitor abolished the cardioprotective effects of tanshinone IIA against H 2 O 2 -induced cell death. Furthermore, western blot analysis demonstrated that tanshinone IIA activated Akt kinase via the phosphorylation of serine 473. Inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway by pretreatment with the PI3K specific inhibitors wortmannin and LY294002 also eliminated the cardioprotective effects of tanshinone IIA against H 2 O 2 -induced cell death. Western blot analysis demonstrated that H 2 O 2 -induced reductions in B cell lymphoma 2 (Bcl-2) expression levels were reversed by tanshinone IIA. In addition, the effect of tanshinone IIA on Bcl-2 protein expression level in an oxidative environment was suppressed by a PI3K inhibitor, wortmannin, indicating that tanshinone IIA exerts cardioprotective effects against H 2 O 2 -induced cell death via the activation of the PI3K/Akt signal transduction pathway and the consequent upregulation of Bcl-2. In conclusion, the present study demonstrates that TIIA is able to protcet H9c2 cells from oxidative stress-induced cell death through signalling pathways involving miR-133 and Akt, and that tanshinone IIA is a promising natural cardioprotective agent.

ObjectiveThe aim of the present study was to assess the association between the 2037T/C and 2237G/A polymorphisms in the EL gene and the risk of CAD and lipid levels in a Chinese population.MethodsA case-control study including 706 patients with CAD and 315 controls was performed. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to identify the genotypes.ResultsThe EL 2037 T/C polymorphism was associated with CAD risk and HDL-C levels. No significant differences were found between the EL 2237 G/A genotypes and CAD risk and lipid levels in the whole population. However, carriers of the 2237 A allele had higher Apo A1 levels than those with the 2237 GG genotype and in the CAD subgroup (P = 0.044). The CAD cases have a significantly lower frequency of the C-G haplotypes than the controls, and the T-A haplotype was significantly more common in the CAD patients than in the controls.ConclusionsOur study concluded that the EL 2037 T/C polymorphism was associated with CAD risk and HDL-C levels, and that the C allele might be a protective factor against CAD in the Chinese Han population. In addition, the EL 2237 A allele might be associated with an increased Apo A1 level in CAD subjects.