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Coronary heart disease is the most common cause of death among diabetic patients. The increased risk of coronary heart disease in type 2 diabetes is due, in part, to lipid abnormalities often present in the diabetic patient. Diabetic dyslipidemia is characterized by elevated triglycerides, low high‐density lipoprotein cholesterol (HDL‐C) and an increased preponderance of small, dense low‐density lipoprotein cholesterol (LDL‐C) particles. Current guidelines for the prevention of coronary heart disease in diabetic patients identify elevated LDL‐C as the primary target of lipid‐lowering therapy, and recommend statins as the first‐line treatment for diabetic dyslipidemia. This review evaluates the large statin trials that have included diabetic patients, and discusses the role of combination therapy in managing dyslipidemia in diabetic patients. Copyright © 2007 Wiley Periodicals, Inc.

Background and aims: Granulocyte-colony stimulating factor (G-CSF) has been shown to exert neuroprotective effects in several in vivo models of brain injury mediated by its anti-apoptotic, antiinflammatory, neurotrophic and excitoprotective action. However, the effect of G-CSF on functional abilities following neonatal hypoxia-ischemia (HI) is still uncertain. The aim of this study was to evaluate the effect of G-CSF on HI-induced long-term behavioral impairment (motor and memory ability) and brain injury.Methods: Seven-day-old rats underwent unilateral, permanent carotid artery ligation followed by 1h of hypoxia and were divided into 3 groups: A (n=7, sham-operated), B (n=14, HI), and C (n=14, HI-GCSF), post-treated with G-CSF (50 µg/ kg). Behavioral tests were performed from days P50-P65, during which motor activity (rota-rod) and learning/memory function (water maze) were examined. Histological analysis was performed at the level of dorsal hippocampus according to a semiquantitative 5-point scale.Results: HI resulted in significant motor function (102.5±14.8sec) and spatial reference (37.4±5.5sec) and working memory impairment (30.8±4sec) compared to sham-operated rats (rota-rod:213±22sec, reference:14.7±1.8 and working memory:14.2±2sec) (p< 0.05). G-CSFtreated rats exhibited significantly improved performance in rota-rod (167.7±14.8sec) and water maze (reference:11.7±1.3 and working memory:17.3±5.5sec) tests, almost reaching the performance of sham-operated animals. Neonatal HI resulted in extensive neuronal damage that was limited after G-CSF administration (p< 0.05).Conclusions: G-CSF administration exerts longterm neuroprotective effect by reducing the HIinduced neuronal injury and neurological deficits. Longer-latency effects implicated in neuroprotective role of G-CSF, such as neurogenesis or neurotrophic action, should be investigated. Background: Propofol is a frequently used drug in pediatric anesthesia and neonatology. We have recently shown that exposure of rodent pups by propofol induces neuronal apoptosis in short term.