Erythropoietin in neonatal brain protection: the past, the present and the future

Over the last decade, neuroprotective effects of erythropoietin (Epo) and its underlying mechanisms in terms of signal transduction pathways have been defined and there is a growing interest in the potential therapeutic use of Epo for neuroprotection. Several mechanisms by which Epo provides neuroprotection are recognized. In this review, we focused on the neuroprotective mechanisms of Epo and provide a short overview on both experimental and clinical studies, testing Epo as a neuroprotective agent in the neonatal brain injury, and the safety concerns with the clinical use of Epo treatment in neonates.     

A perspective on the ESVEM trial and current knowledge: Catheter ablation for ventricular tachyarrhythmias

Although an effective and potentially curative technique for treating idiopathic ventricular tachycardia, map-guided transcatheter radiofrequency ablation is far from optimal for ventricular tachyarrhythmias in patients with advanced ischemic or other types of organic heart disease. First, this technique can be applied only to a minority of patients with structural heart disease, who can tolerate relatively long episodes of induced ventricular tachycardia necessary for mapping and successful ablation. Second, the success rate is lower and recurrence higher in patients with organic heart disease. Finally, for patients who lose consciousness during tachycardia or who present with prehospital cardiac arrest, transcatheter radiofrequency ablation is inappropriate as definitive treatment. At best, it is palliative and may be used to suppress relatively slow, frequent, or incessant ventricular tachycardias but does not obviate the need for other therpaies such as cardioverter-defibrillator implantation or antiarrhythmic drug therapy.     

Suppression of the onset of myelination extends the permissive period for the functional repair of embryonic spinal cord.

In an embryonic chicken, transection of the thoracic spinal cord prior to embryonic day (E) 13 (of the 21-day developmental period) results in complete neuroanatomical repair and functional locomotor recovery. Conversely, repair rapidly diminishes following a transection on E13-E14 and is nonexistent after an E15 transection. The myelination of fiber tracts within the spinal cord also begins on E13, coincident with the transition from permissive to restrictive repair periods. The onset of myelination can be delayed (dysmyelination) until later in development by the direct injection into the thoracic cord on E9-E12 of a monoclonal antibody to galactocerebroside, plus homologous complement. In such a dysmyelinated embryo, a subsequent transection of the thoracic cord as late as E15 resulted in complete neuroanatomical repair and functional recovery (i.e., extended the permissive period for repair).