In other words, our study showed that intact endothelial function in the anterior cerebral and systemic circulation could not be only

associated with migraine but again this could be also attributed to GSK2118436 in vivo physiological conditions. This again is in accordance with one of our previous findings that migraine patients without comorbidities and early atherosclerotic process probably have intact systemic endothelial function [8]. This has also been suggested by Vanmolkot and de Hoon [28]. In recent years it has been proposed that migraine is associated with disorders of the coronary, retinal and peripheral vasculature [1]. However, in many studies the authors did not exclude vascular risk factors, or perhaps they excluded many vascular risk factors, but did not evaluate IMT, a morphological marker of the early atherosclerotic process and associated endothelial dysfunction, which consequently might have biased their findings [2], [3], [4], [5], [6] and [7]. Therefore, according to the previous sentence, the findings of our current and previous studies might suggest that behind vascular disorders could not be systemic endothelial dysfunction BGB324 price but perhaps localized

endothelial dysfunction or other pathological vascular conditions. Taking into account all the presented findings of this and previous studies, the following can be concluded in migraine patients without comorbidities: (I) impaired endothelial function in the posterior cerebral circulation is associated with migraine; (II) intact endothelial function in the anterior cerebral PRKD3 and systemic circulation is not associated only with migraine. The authors express their gratitude to Valentin Beznik and Marjeta Švigelj for technical assistance, and especially to all the volunteers. “
“Given the narrow therapeutic time window for reperfusion in acute ischemic stroke, there is a strong need for neuroprotective

strategies aiming at preservation of tissue at risk for infarction to increase the number of patients eligible for reperfusion. Former clinical trials in neuroprotection led to disappointing results due to poor interpretation and translation from an experimental to a clinical setting. When selecting agents for neuroprotection not only proof of efficacy but also easy implementation in acute stroke care is of great importance. Gas therapy and especially the noble gas helium might be a promising neuroprotective strategy that meets criteria for every day practical use [1], [2] and [3]. Helium is directly available in the hyperacute prehospital phase, is well-tolerated and lacks toxicity or interactions [4] and [5]. The exact neuroprotective mechanism of helium is not well known but egression of nitrogen from neural mitochondria is suggested. This might facilitate oxygen reuptake during reperfusion [6]. Another supposed mechanism of neuroprotection by gas therapy is an increase of cerebral blood flow.