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To conclude, the present study suggests that simvastatin per se protects the neurons in hippocampus and frontal cortex from AlCl3, an environmental toxin.
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QRQYG could stabilize the vulnerable plaque through inhibition of the inflammatory response.
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Textual information was preferred but numerical information, in particular in the form of a natural frequency, may help patients make judgements about their medicines. NNTs were found to be very difficult to understand. This raises the prospect that some patients might reject medicines because of disappointment with the perceived low benefits of their medicines. The self-reported impact on behaviour appeared minimal with reports of intentions to 'do what the doctor tells me'. Further research is needed to explore the impact of such statements on people who are yet to be prescribed a statin.
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We conclude that simvastatin has a major antiproliferative effect on AML blasts in vitro. Also, the combination of simvastatin and ARA-C significantly enhanced the antiproliferative effect of each drug. These findings may open new avenues in both the laboratory and clinical research of the treatment of leukemia.
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We identified 601 DDI-ADE pairs for the three drugs using the filtering pipeline, of which 61 pairs are in Grade 5, 56 pairs in Grade 4 and 484 pairs in Grade 3. Among 601 pairs, the signals of 59 DDI-ADE pairs were identified from the EMR data.
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Human embryonic kidney cells HEK-293T and human pancreatic cancer cells MiaPaCa-2 were treated with simvastatin (6 and 12 μM) for 24 and 48 hours respectively. Neutral lipid probe Nile Red was used for detection of LDs by fluorescence microscopy. Cellular cholesterol content was determined by HPLC. Changes in expression of genes related to lipid metabolism in simvastatin-treated MiaPaCa-2 cells were examined by DNA microarray analysis. Validation of gene expression changes was performed using quantitative RT-PCR.
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Statins have numerous potential benefits relevant to abdominal surgery, and their use has been associated with a reduction in the systemic inflammatory response syndrome, wound infection, and anastomotic leak after colorectal surgery. However, this clinical evidence is limited to retrospective studies. The aim of this study was to prospectively investigate whether perioperative statin therapy can decrease the incidence of complications after major colorectal surgery.
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The available results from these three trials do not provide credible evidence of any adverse effect of ezetimibe on rates of cancer. Follow-up of longer duration will permit the balance of risks and benefits to be determined more reliably.
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Granulocyte colony-stimulating factor (G-CSF), a hematopoietic cytokine, was recently used to treat patients of acute myocardial infarction with beneficial effect. However, controversy exists as some patients developed re-stenosis and worsened condition post G-CSF delivery. This study presents a new disease model to study G-CSF induced cardiac thrombosis and delineate its possible mechanism. We used iron loading to mimic condition of chronic cardiac dysfunction and apply G-CSF to mice to test our hypothesis.
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Our first results correspond to results of other authors. We also compared results with fluvastatin with our previous studies in which we used lovastatin and simvastatin. From the comparision with other statins we can conclude that the efficacy of fluvastatin is similar to lovastatin and simvastatin. On the other hand we have to notice, that the percent reduction of total and LDL-cholesterol after fluvastatin was a little bit smaller.
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We analyzed the relation between LDL and HDL cholesterol levels to predict the risk of future coronary events. Using data from the Lipid Research Clinics Follow-up Cohort, we developed multivariate equations to predict coronary deaths among 4684 men and women followed for approximately 12 years. We used these equations to compare the predictive power of the LDL/HDL ratio with the independent effects of LDL and HDL and an LDL-HDL interaction term. We then used each model to forecast the 10-year risk of coronary death based on various lipid levels after adjustment for conventional risk factors (eg, blood pressure, gender, cigarette smoking).
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Statins are effective and often-prescribed drugs for the treatment of hypercholesterolemia. This study shows a simple and fast method validation by reversed-phase high-performance liquid chromatography in the linear range 28 to 52 µg/mL to quantify lovastatin, pravastatin sodium or simvastatin in bulk drug or dosage forms. Statins were determined using a C8 endcapped column (250 × 4 mm, 5 µm), isocratic mobile phase of acetonitrile and 0.1% phosphoric acid (65:35), 30°C, ultraviolet-diode array detection at λ 238 nm and 1.5 mL/min flow for lovastatin and simvastatin and 1.0 mL/min for pravastatin sodium. The developed method is fast, simple, reliable and shows appropriate linearity (r > 0.999), accuracy (98.8-101.6%), precision (relative standard deviation <2%) and selectivity toward placebo and/or degradation products in very similar chromatographic conditions for all statins.
An early benefit was seen in PROVE IT but not in A to Z. Late-phase results were similar. Factors that may explain this disparity include the intensity of therapy in the early phase, timing, and magnitude of LDL and C-reactive protein lowering, differences in early revascularization, and the play of chance. Taken together, the results of these trials support a strategy of early intensive statin therapy coupled with revascularization when appropriate in patients after acute coronary syndrome.
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Type 2 DM is associated with increased postprandial lipemia and abnormal lipid homeostasis. Lipid intolerance detected in a postprandial lipemia test may be an indication for hypolipemic therapy.
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The two groups with HFD showed more than 25% increase in weight at the end of study as compared to control group. HFD group showed significantly higher lipid profile and decreased sciatic nerve conduction velocity when compared with control. The group that was given Simvastatin showed significant improvement in lipid profile and increased sciatic nerve conduction velocity after 4 weeks when compared with the group that was given HFD without any intervention.
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Angiotensin II (Ang II) is involved in the pathogenesis of atrial fibrillation (AF). L-type calcium channel (LCC) expression is altered in AF remodeling. We investigated whether Ang II modulates LCC current through transcriptional regulation, by using murine atrial HL-1 cells, which have a spontaneous calcium transient, and an in vivo rat model. Ang II increased LCC alpha1C subunit mRNA and protein levels and LCC current density, which resulted in an augmented calcium transient in atrial myocytes. An approximately 2-kb promoter region of LCC alpha1C subunit gene was cloned to the pGL3 luciferase vector. Ang II significantly increased promoter activity in a concentration- and time-dependent manner. Truncation and mutational analysis of the LCC alpha1C subunit gene promoter showed that cAMP response element (CRE) (-1853 to -1845) was an important cis element in Ang II-induced LCC alpha1C subunit gene expression. Transfection of dominant-negative CRE binding protein (CREB) (pCMV-CREBS133A) abolished the Ang II effect. Ang II (1 micromol/L, 2 hours) induced serine 133 phosphorylation of CREB and binding of CREB to CRE and increased LCC alpha1C subunit gene promoter activity through a protein kinase C/NADPH oxidase/reactive oxygen species pathway, which was blocked by the Ang II type 1 receptor blocker losartan and the antioxidant simvastatin. In the rat model, Ang II infusion increased LCC alpha1C subunit expression and serine 133 phosphorylation of CREB, which were attenuated by oral losartan and simvastatin. In summary, Ang II induced LCC alpha1C subunit expression via a protein kinase C-, reactive oxygen species-, and CREB-dependent pathway and was blocked by losartan and simvastatin.
Diabetic patients were identified using two different classifications schemes: Clinical history (diabetic, non-diabetic) and the new American Diabetes Association definition (diabetic, impaired fasting glucose, normal fasting glucose). The analysis is based on prospectively collected data from the trial on hospitalization for cardiovascular problems, study drug utilization and mortality. The incremental cost per life year saved with simvastatin is estimated using costs from Sweden (primary) and other European countries.
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The study included 50 children with FH (9 to 18 years) and 19 healthy, non-FH controls. Children with FH were randomized to receive simvastatin or placebo for 28 weeks. The FMD was performed at baseline and at 28 weeks of treatment.
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Major improvements in medical therapy and percutaneous coronary intervention (PCI) for coronary heart disease have occurred during the past decade, but no randomized trial has compared these 2 strategies for the "hard" clinical end points of death or myocardial infarction nor have earlier studies incorporated the use of coronary stents and aggressive multifaceted medical therapy during long-term follow-up.
The safety and tolerability of rosuvastatin were assessed using data from 16,876 patients who received rosuvastatin 5-40 mg in a multinational phase II/III/IIIb/IV program, representing 25,670 patient-years of continuous exposure to rosuvastatin.
Statins are commonly used antihyperlipidemic agents, with anti-inflammatory and immunomodulatory properties that are thought to account for a significant portion of their ability to protect against atherosclerosis and cardiovascular disease. Vaspin, a visceral adipose tissue-derived serine protease inhibitor, is an emerging adipokine with important insulin-sensitizing, cardioprotective, and antiatherosclerotic properties in patients with diabetes. In this randomized controlled clinical trial, we evaluated the effect of statin therapy on vaspin levels in patients with type 2 diabetes mellitus.
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Increases in arginase activity have been reported in a variety of disease conditions characterized by vascular dysfunction. Arginase competes with NO synthase for their common substrate arginine, suggesting a cause and effect relationship. We tested this concept by experiments with streptozotocin diabetic rats and high glucose (HG)-treated bovine coronary endothelial cells (BCECs). Our studies showed that diabetes-induced impairment of vasorelaxation to acetylcholine was correlated with increases in reactive oxygen species and arginase activity and arginase I expression in aorta and liver. Treatment of diabetic rats with simvastatin (5 mg/kg per day, subcutaneously) or L-citrulline (50 mg/kg per day, orally) blunted these effects. Acute treatment of diabetic coronary arteries with arginase inhibitors also reversed the impaired vasodilation to acetylcholine. Treatment of BCECs with HG (25 mmol/L, 24 hours) also increased arginase activity. This effect was blocked by treatment with simvastatin (0.1 micromol/L), the Rho kinase inhibitor Y-27632 (10 micromol/L), or L-citrulline (1 mmol/L). Superoxide and active RhoA levels also were elevated in HG-treated BCECs. Furthermore, HG significantly diminished NO production in BCECs. Transfection of BCECs with arginase I small interfering RNA prevented the rise in arginase activity in HG-treated cells and normalized NO production, suggesting a role for arginase I in reduced NO production with HG. These results indicate that increased arginase activity in diabetes contributes to vascular endothelial dysfunction by decreasing L-arginine availability to NO synthase.
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For high-risk patients who do not achieve guideline-recommended LDL-C levels, more intensive treatment including statin-uptitration to higher doses or potency, as well as combination therapy may be considered. A better understanding of statin treatment patterns in real-world clinical practice may contribute to improved lipid-lowering management in these patients.
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Combination therapy with a statin and a fibrate is one of the treatment options to manage multiple lipid abnormalities in patients with hypercholesterolemia and elevated TGs.
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Simvastatin is widely used in the treatment of hypercholestero-lemia. Recently, it was reported that it is also effective in reducing lethality in coronary heart disease. A simple and sensitive reversed-phase liquid chromatographic method has been developed and validated for the analysis of simvastatin in human plasma. Simvastatin and internal standard lovastatin in plasma were extracted with cyclohexane-dichloromethane (3.5:1, V/V), and then measured by HPLC using a Lichrospher C18 column as stationary phase and an acetonitrile-water (70:30, V/V) mixture as mobile phase. The flow rate was 1.2 mL/min. Simvastatin was quantified by UV at 237 nm. The calibration curve showed a good linearity in the mass concentration range of 0.25-50.0 micrograms/L. The regression equation is: Y = 0.0364 rho + 0.00583, r = 0.9998. Intra-day and inter-day coefficients of variation of assay for simvastatin in plasma < 7.94% and < 8.58%, respectively. The recoveries of simvastatin were > 93.3%. The method has been used to determine simvastatin in plasma from 12 healthy male volunteers.
Results from previous investigations have indicated that glucose-stimulated insulin secretion (GSIS) is affected by changes in cholesterol and its intermediates, but the precise link between secretion and cholesterol has not been thoroughly investigated. In this study, we show the contribution of both protein isoprenylation and cholesterol-dependent plasma membrane structural integrity to insulin secretion in INS-1E cells and mouse islets. Acute (2 h) inhibition of hydroxyl-methylglutaryl-CoA reductase by simvastatin (SIM) resulted in inhibition of GSIS without reduction in total cellular cholesterol content. This effect was prevented by cell loading with the isoprenyl molecule geranylgeranyl pyrophosphate. Chronic (24 h) inhibition of cholesterol biosynthesis resulted in inhibition of GSIS with a significant reduction in total cellular cholesterol content, which was also observed after the inhibition of cholesterol biosynthesis downstream of isoprenoid formation. Electron paramagnetic resonance analyses of INS-1E cells showed that the SIM-induced reduction in cholesterol increased plasma membrane fluidity. Thus, the blockade of cholesterol biosynthesis resulted in the reduction of availability of isoprenoids, followed by a reduction in the total cholesterol content associated with an increase in plasma membrane fluidity. Herein, we show the different contributions of cholesterol biosynthesis to GSIS, and propose that isoprenoid molecules and cholesterol-dependent signaling are dual regulators of proper β-cell function.