ERYTHROPOIETIN FOR THE TREATMENT OF SUBARACHNOID HEMORRAGE: A FEASIBLE INGREDIENT FOR A SUCCESS MEDICAL RECIPE

Subaracnhoid hemorrage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents. Althoug an aneurysm can be effectively managed by surgery or endovascular therapy, delayed cerebral ischemia is diagnosed in a high percentage of patients resulting in significant morbility and mortality. Cerebral vasospasm occurs in more than half of all patients after aneurysm rupture and is recognized as the leading cause of delayed cerebral ischemia after SAH. Hemodynamic strategies and endovascular procedures may be considered fo the treatment of cerebral vasospasm. In recent years, the mechanism contributing to the development of vasospasm, abnormal reactivity of cerebral arteries and cerebral ischemia following SAH, have been intensively investigated. A number of pathological processes have been identified in the pathogenesis of vasospasm including endothelial injury, smooth muscle cell contraction from spasmogenic substances produced by the subarachnoid blood clots, changes in vascular responsiveness and inflammatory response of the vascular endothelium. to date, the current therapeutic interventions remain ineffective being limited to the manipulation os systemic blood pressure, variation of blood volume and viscosity, and control of arterial carbon dioxide tension. In this scenario, the hormone erythropoietin (EPO), has been found to exert neuroprotective action during experimental SAH when its recombinant form (rHuEPO) is systematically administered. However, recent translation of experimental data into clinical trials has suggested an unclear role of recombinant human EPO in the setting of SAH. In this context, the aim of the recurrent review is to present current evidence on the potential role of EPO in cerebrovascular dysfunction following aneurysmal subarachnoid hemorrage

Properties of textile air conditioner waste dust-filled polyurethane rigid foam composites

This paper investigates the morphology, mechanical and thermal insulation properties of textile air conditioner dust-filled polyurethane (PU) rigid foams. Textile air conditioner dust occurs during the spinning process of staple fibres. It consists of cotton fibre impurities as boll, leaf, and short fibres that generate a vast environmental load. This dust is used as a filler and dispersed in polyurethane up to 40% wt. The cell -size of foams decreased and cell -density increased by the increase in filler ratios in which the dust acted as a heterogeneous nucleation site during cell formation. The dust agglomerated in polyurethane foam and induced irregular cell wall and hence non-uniform cell formation and many broken cells. The flexural strength and modulus decreased in higher dust content (40% wt.). The lower thermal insulation of cellulose-based dust and damaged structure/uniformity of foam cells resulted in an unstable/lower thermal conductivity of dust-filled polyurethane rigid foam composites