DI, AB and MD performed clinical psychologist interventions. MLM, AB, MD, DI, EV, MS, IB, EB and IB performed follow-up examinations. http://www.selleckchem.com/products/epz-5676.html GZ performed statistical analysis. AP, DI, AB and GZ wrote the draft. All Authors revised the manuscript and approved the final version.AcknowledgementsThe Clinical Psychological Service is supported by institutional public funds (Florence Health Society, Tuscany Region, Careggi Teaching Hospital).
Stroke, a growing epidemic, remains a leading cause of mortality and disability worldwide [1-3]. Surprisingly, while the epidemiology, etiologies, mechanisms, classification, and prognostic outcomes of ischemic stroke (IS) have been widely investigated for several decades, a safe and effective treatment strategy for patients after acute IS has not been fully developed [4-8].

Recently, thrombolysis using tissue plasminogen activator (tPA), a more aggressive management strategy, has been shown to be effective for some acute IS patients early after the onset of symptoms [9,10]. However, tPA use is hampered by many limitations in daily clinical practice [10-13]. In addition to its narrow indication for only a small number of patients, tPA therapy has been reported to have a relatively high incidence of intracranial bleeding complications [13,14]. The majority of acute IS patients, therefore, are still left without any specific treatment. Hence, finding a safe and effective therapeutic regimen for patients following acute IS, especially those unsuitable for thrombolytic therapy, is of utmost importance for physicians.

Erythropoietin (EPO) was originally used for treating anemic patients of various etiologies, especially for patients with uremia. Interestingly, in addition to its role in normalizing erythropoiesis, EPO has been clearly shown to exert a myocardial protective effect against ischemia-related damage [15-17]. In contrast, the neuroprotective effect of EPO after acute IS is not well-documented and the results are inconsistent [18-20]. The mechanisms underlying the anti-ischemic action of EPO have been proposed to involve anti-apoptotic processes [15,16], neovascularization, mobilization of endothelial progenitor cells (EPCs), and angiogenesis [21-23]. An increase in circulating levels of EPCs in patients after acute IS has been demonstrated to be strongly associated with favorable clinical outcomes in our recent study [24].

Accordingly, we proposed that other than its role in protecting myocardium against ischemic insult, EPO therapy may enhance the circulating Anacetrapib EPC level and improve neurological function and clinical outcome in patients after acute IS.Materials and methodsStudy designThis clinical trial was approved by the Institutional Review Committee on Human Research in Chang Gung Memorial Hospital (No 96-1381A) in 2007 and conducted at Kaohsiung Chang Gung Memorial Hospital.This was a prospective, randomized, and placebo-controlled trial.