EC-SOD overexpression to the lung ameliorated MCT-induced PH in rats. We suggest that EC-SOD may act as an antioxidant in PH and that increased oxidative stress may be important in the pathogenesis of MCT-induced PH.

Accumulating evidence has shown that seasonal variations can exist within metabolic syndrome parameters. The aim of this study was to examine the hypothesis that there are seasonal variations in the prevalence of metabolic syndrome in Japanese subjects. We investigated a total of 1202 male workers in our institution (44 ± 10 years) who underwent health checkups in both June (summer) and December (winter) 2008. In this study, metabolic syndrome was defined according to the criteria proposed by the National Cholesterol Education Program (NCEP), the International Diabetes Federation (IDF) and the Japanese Society of Internal Medicine (JSIM). Serum levels of high-density lipoprotein-cholesterol and fasting glucose, as well as blood pressure (BP), were significantly higher in winter than in summer, whereas waist circumference and serum levels of triglyceride exhibited little change. The prevalence rates of NCEP, IDF, and JSIM metabolic syndrome in this study were 3.8, 15.1 and 12.4% in winter and 3.2, 10.7 and 8.4% in summer, respectively. Of all metabolic syndrome components, an elevated BP was most significantly correlated with the seasonal variation of metabolic syndrome prevalence. This study demonstrated seasonal variations in metabolic syndrome prevalence in Japanese male workers. These results indicate that the season of health checkups may affect the clinical diagnosis and management of metabolic syndrome.

Aim: High-sensitivity C-reactive protein (hsCRP) is a predictor of cardiovascular events. Although oxidative stress may also be related to cardiovascular disease, there are few studies comparing the two. We therefore examined the association of hsCRP, serum lipids, and derivatives of reactive oxygen metabolites (D-ROMs) in coronary artery disease. Methods: We measured the levels of serum lipids, hsCRP, plasma brain natriuretic peptides (BNP) and D-ROMs in 131 consecutive patients undergoing cardiac catheterization. We divided these subjects into three groups according to their levels of hsCRP.

reduces cuff-induced neointima formation and proinflammatory cytokines. Am J Physiol Heart Circ Physiol 292: H2824 -H2831, 2007. First published February 2, 2007; doi:10.1152/ajpheart.01221.2006.-An inflammatory response followed by vascular injury plays an important role in neointima formation and development of atherosclerotic lesions, which are in part mediated by proinflammatory cytokines. Using a cuff injury model, we examined the effects of adenovirusmediated overexpression of phosphatase and tensin homology deleted on chromosome 10 (PTEN) on neointima formation and the proinflammatory response. A cuff was placed around the femoral artery, and adenovirus expressing human PTEN type 1 (AdPTEN) or Escherichia coli ␤-galactosidase (AdLacZ) was injected between the cuff and the adventitia. After 14 days, the arteries were examined histopathologically and by Western blotting. The significant reduction of neointima formation by AdPTEN compared with AdLacZ was accompanied by reduced cell proliferation and increased adventitial cell apoptosis. AdPTEN also reduced expression of phosphorylated IB-␣, but not nonphosphorylated IB-␣. Western blotting revealed that AdPTEN reduced the cuff injury-induced expression levels of monocyte chemoattractant protein-1, TNF-␣, and IL-1␤ and their expression in all layers of the arterial wall. In contrast, cuff-induced macrophage invasion, which was also inhibited by AdPTEN, was detected only at the intimal surface and in the adventitia. In cultured vascular smooth muscle cells, PTEN directly inhibited ANG IIinduced monocyte chemoattractant protein-1 expression as quantified by real-time PCR and Western blotting. Our results suggest that overexpression of PTEN reduces neointima formation, possibly in part through inhibition of the inflammatory response by macrophage invasion and proinflammatory cytokine expression. vascular inflammation; monocyte chemoattractant protein-1; gene transfer PHOSPHATASE AND TENSIN homology deleted on chromosome 10 (PTEN) is a multifunctional lipid phosphatase that was originally identified as a tumor suppressor gene (20,22). In addition to its tumor suppression capability, it is also known to modulate several cell functions, including migration, proliferation, and apoptosis (36). These actions of PTEN are mediated by antagonism of the phosphatidylinositol 3-kinase (PI3K)-mediated signaling pathway (22). Moreover, PTEN also has protein tyrosine phosphatase activity, which downmodulates signaling pathways involving focal adhesion kinase (FAK) or Shc (34,36). Modulation of FAK/Shc activity by PTEN affects cell migration and adhesion activated by integrins and other tyrosine kinase receptors (34, 36). PTEN has recently been found to play an essential role in cells of the cardiovascular system (25). PTEN is expressed endogenously and regulates many cell functions in cardiomyocytes, fibroblasts, endothelial cells, and vascular smooth muscle cells (VSMCs), including proliferation, migration, survival/apoptosis, hypertrophy, contractility, metabolism, and mechan...