Serum omentin-1 levels were found to be significantly decreased in patients with Type 2 diabetes (19.7 ± 1 ng/ml) and in patients with Type 2 diabetes with ischaemic heart disease (18.5 ± 1.6 ng/ml) compared with healthy control subjects (27.4 ± 2.6 ng/ml) at P < 0.01. Moreover, serum chemerin levels were found to be significantly increased in patients with Type 2 diabetes (347 ± 14 ng/ml) and in patients with Type 2 diabetes with ischaemic heart disease (341 ± 16.5 ng/ml) compared with healthy control subjects (281 ± 13 ng/ml) at P < 0.01. Interestingly, omentin-1 and chemerin levels were found to be significantly correlated negatively with each other as well as being individually correlated with some selected anthropometric, biochemical and clinical variables. In conclusion, both omentin-1 and chemerin might play as a pivotal role in obesity and its associated disorders as Type 2 diabetes; however, their role in cardiovascular diseases needs to be fully elucidated.

Glioblastoma multiforme (GBM) tumors are the most common malignant primary brain tumors in adults. Although many GBM tumors are believed to be caused by self-renewing, glioblastoma-derived stem-like cells (GSCs), the mechanisms that regulate self-renewal and other oncogenic properties of GSCs are only now being unraveled. Here we showed that GSCs derived from GBM patient specimens express varying levels of the transcriptional repressor REST, suggesting heterogeneity across different GSC lines. Loss- and gain-of-function experiments indicated that REST maintains self-renewal of GSCs. High REST-expressing GSCs (HR-GSCs) produced tumors histopathologically distinct from those generated by low REST-expressing GSCs (LR-GSCs) in orthotopic mouse brain tumor models. Knockdown of REST in HR-GSCs resulted in increased survival in GSC-transplanted mice and produced tumors with higher apoptotic and lower invasive properties. Conversely, forced expression of exogenous REST in LR-GSCs produced decreased survival in mice and produced tumors with lower apoptotic and higher invasive properties, similar to HR-GSCs. Thus, based on our results, we propose that a novel function of REST is to maintain self-renewal and other oncogenic properties of GSCs and that REST can play a major role in mediating tumorigenicity in GBM.

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This study compared lipids, the product of lipid peroxidation malondialdehyde (MDA), the acute phase reactant high-sensitive C-reactive protein (hsCRP), endothelin-1 (ET-1), P-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) between healthy controls, subjects with ischemic heart disease (IHD) and type 2 diabetes mellitus (DM) subjects who did not perform coronary artery bypass graft (CABG) surgery as well as type 2 DM subjects who performed CABG. HbA1c, lipids, MDA, hsCRP, ET-1, P-selectin, ICAM-1, and VCAM-1 levels were significantly higher in the diabetic groups than in either healthy controls or IHD subjects. In the diabetic groups, there was a negative association among hsCRP and HDL-C. ET-1, ICAM-1 levels, and TAG were positively correlated, as do the association between P-selectin, VCAM-1, and HbA1c%. Also a positive relation was found among hsCRP levels and ICAM-1, as well as MDA and ET-1. P-selectin and ICAM-1 were significantly positively correlated. This study indicates that increased level of oxidative stress marker, proinflammatory markers, and their downstream effectors adhesion molecules occur in type 2 DM.

Soluble forms of the receptor for advanced glycation end product could be an endogenous protection factor against occurrence of DF, hence may be of therapeutic value in the treatment of DF.

Adipose tissue can release proinflammatory mediators, namely C-reactive protein (CRP), interleukin 1β (IL-1β), and monocyte chemotactic protein 1 (MCP-1), contributing to vascular injury and insulin resistance (IR). Other mediators namely, adiponectin and nitric oxide (NO) are protective. We enrolled type 2 diabetes mellitus (T2DM) obese male patients without coronary heart disease ([CHD] group II, n = 25) and T2DM obese patients with CHD (group III, n = 25). They were compared with 20 age- and body mass index (BMI)-matched nondiabetic control males (group I). Fasting blood glucose (FBG), glycated hemoglobin (HbA(1c)%), lipids, insulin, malondialdehyde ([MDA]; lipid peroxidation product), NO, high-sensitivity CRP (hsCRP), IL-1β, MCP-1, adiponectin as well as sE-selectin concentration were significantly different in patients with T2DM and CHD compared with patients without CHD and nondiabetic controls (P = .01). There was a significant negative correlation between adiponectin and E-selectin (P = .0001). Adipose tissue in T2DM obese patients may contribute to the pathogenesis of CHD.

Background/Aim: High incidence of cardiovascular disease (CVD) in chronic kidney disease (CKD) patients is a result of an interlaced relation between oxidative stress, endothelial dysfunction (ED) and inflammation. This study tries to investigate the development of these processes in CKD patients receiving conservative treatment or on hemodialysis (HD). We also examined the modulating effect of oral L-arginine in HD patients having CVD. Methods: The study included 12 healthy volunteers and 63 renal patients divided into 15 renal impairment, 18 HD free of CVD, and 30 HD suffering from CVD (HD+CVD). Of the latter, 15 patients were given oral L-arginine (15 g/day, 5 g t.i.d.) for 1 month. Blood levels of asymmetric dimethylarginine (ADMA), malondialdehyde (MDA), and homocysteine and myeloperoxidase activity (MPO) were estimated. Results: ADMA, MDA and homocysteine were significantly elevated in renal impairment group. HD and HD+CVD patients experienced higher levels, along with high MPO activity. Significant reduction by 21, 46, 11, and 26%, respectively, in the aforementioned parameters was observed in HD+CVD patients following L-arginine intake. Conclusion:We recommend considering ADMA, MDA, homocysteine and MPO as potentially important cardiovascular risk factors in CKD patients, and focus the attention to the cardiovascular advantages of L-arginine in these patients.