Association of shorter mean telomere length with large artery stiffness in patients with coronary heart disease.

BACKGROUND: Accumulating evidence implicates leukocyte telomere length (LTL) shortening as a potential risk predictor for cardiovascular disease. Arterial stiffness chronicles the cumulative burden of cardiovascular disease risk factors. Therefore, the capacity of LTL to predict arterial stiffness was examined. METHODS: A total of 275 unrelated Chinese males: 163 patients with coronary artery disease (CAD) and 112 healthy controls, 40-73 years of age were included in this study. The relative telomere length of leukocytes was determined by a real-time fluorescence quantitative polymerase chain reaction (PCR). Large artery stiffness was measured with carotid-femoral pulse wave velocity (PWV). RESULTS: The relative telomere length (T/S) ratio was significantly shorter in patients with CAD (0.79 +/- 0.26) than in control subjects (1.08 +/- 0.22) (p<0.001). The correlation between LTL and PWV in patients with CAD was stronger than that in the controls (r= -0.467, r(2)=0.227, p<0.001 for patients with CAD versus r= -0.223; r(2)=0.050; p=0.018 for controls). The log(e)-transformed T/S ratio was inversely correlated with age (r= -0.345; p<0.001), PWV (r= -0.326; p<0.001) and C-reactive protein ( r= -0.133; p=0.027). CONCLUSIONS: The data show an association of leukocyte telomere length shortening with increased arterial stiffness and cardiovascular burden, suggesting that telomere length is a biomarker of large artery elasticity and CAD. Further studies are warranted to study the role of LTL dynamics in the pathogenesis of atherosclerosis.

The effects of lead exposure on placental NF-kappaB expression and the consequences for gestation.

The present study was designed to investigate the toxicity of lead exposure on the placenta at different dosages and the relationship with placental expression of NF-kappaB. A total of 67 unrelated Han Chinese pregnant women and 108 Wistar rats were included in this study. The rats were randomly divided into four groups for consumption of water with or without 0.025% lead acetate during various gestational periods; blood samples and placenta were harvested for analysis. Blood lead content was determined by atomic absorption spectrophotometry. Placental NF-kappaB expression was evaluated by immunohistochemistry. Placental cytoarchitecture was examined by histopathology and electronic microscopy. Fetal body weight, body length and placental weight was significantly lower (p<0.05) in the lead-exposed rats compared to controls. Maternal blood lead levels in the rats negatively correlated with placental weight (r=0.652, p<0.01). Rat placenta showed focal necrosis in the decidua with trophoblast degeneration and fibrin deposition. Mitochondria were swollen and decreased in number, rough endoplasmic reticula were distended and ribosomal number on membranes decreased. In the human placenta, we did not find abnormal cytoarchitecture. On the other hand, placental expression of NF-kappaB in lead-exposed rats was significantly higher than that in controls and the expression of NF-kappaB in human placenta was positively correlated with maternal blood lead levels (r=0.663, p<0.01). These findings suggest that lead exposure at various gestational periods produce varied effects, with NF-kappaB activation following lead exposure. Injury to cytoplasmic organelles may interfere with the nutrition and oxygen exchange between mother and fetus, which may be contribute to abnormal pregnancy outcomes.