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Metabolic modulation with perhexiline in chronic heart failure: a randomized, controlled trial of short-term use of a novel treatment.

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Luminal iron levels govern intestinal tumorigenesis after Apc loss in vivo.

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However, therapeutic procedures are performed not only to prevent events but also to improve health status.

CCR6, the sole receptor for the chemokine CCL20, promotes spontaneous intestinal tumorigenesis.

Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trials.

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Because ischaemic heart disease is associated with increased risk for ventricular arrhythmias, the effects of ranolazine during severe left anterior descending coronary artery (LAD) stenosis were assessed in the intact porcine model.

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Ranolazine does not cause deleterious changes in laboratory parameters.

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Ranolazine has been demonstrated to improve exercise time to angina or 1 mm of ST-segment depression in a manner similar to currently approved drugs, but without any significant effects on heart rate or blood pressure at rest or during exercise.

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Similarly, current CABG techniques, including the more frequent use of arterial conduits, were not included in either trial.

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First, direct interference by ranolazine on the HbA 1c assay was investigated and eliminated in experiments measuring HbA 1c in the presence or absence of ranolazine (Gilead Sciences, data on file).

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Extensive observational data before and after the identification of disease-associated genes have shown superior survival among symptomatic patients who received beta-blockers (or occasionally among those who underwent left stellate ganglionectomy) as compared with those who did not.

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Although ranolazine increased FBF acutely, this effect was transient and FBF promptly returned back to baseline (within 15 min) and remained stable afterwards ().

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The primary efficacy end point of the trial was the first occurrence of any element of the composite of cardiovascular death, myocardial infarction, or recurrent ischemia.

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E-4031 (60 nanomolar (nM)), an I Kr inhibitor, induced spontaneous and 3-sec pause-triggered episodes of TdP.

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Mouse genetics suggests cell-context dependency for Myc-regulated metabolic enzymes during tumorigenesis.

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