Temporal spectrum holes exist in the gray

region, where secondary users (SUs) can opportunistically access the licensed spectrum with interweave spectrum sharing. In the white region, SUs can exploit spatial spectrum opportunities and transmit at any time by taking advantage of their long distances from the primary users (PUs), without causing severe interference to PUs. Moreover, the existence condition of the transition zone between the gray region and the white region is theoretically analyzed, where power control should be implemented in SUs. Closed-form bounds of three regions are obtained, which can be YH25448 used in space-time spectrum sensing and access in CRNs. Finally, we provide numerical results to evaluate the relations among the key parameters

in the three regions.”
“In rat tail artery, short trains of electrical stimuli evoke both ATP-mediated excitatory junction potentials (EJPs) and a slow noradrenaline (NA)-mediated depolarization AP26113 cell line (NAD). Here we have investigated the contribution of alpha(1)- and alpha(2)-adrenoceptors to the NAD. The aradrenoceptor antagonist, prazosin (0.1 mu M), and the alpha(2)-antagonist, rauwolscine (1 mu M), reduced the amplitude of the NAD and in combination these agents virtually abolished the NAD. The K-ATP, channel blocker, glibenclamide (10 mu M) abolished the alpha(2)-adrenoceptor-mediated component of the NAD, indicating that activation of these receptors produces closure of K-ATP channels. The alpha(1)-adrenoceptor-mediated component of the NAD was increased in amplitude by glibenclamide. Changes in membrane conductance were monitored by measuring the time constant of decay of EJPs (tau EJP). The tau EJP was increased during alpha(1)-adrenoceptor-mediated depolarization, indicating a decrease

in membrane conductance; i.e. closure of K+ channels. Broad-spectrum K+ channel blockers (tetraethylammonium, 4-aminopyridine, Ba2+) and the TASK-1 K+ channel blocker, anandamide (10 mu M), did not reduce the alpha(1)-adrenoceptor-mediated NAD. The alpha(1)-adrenoceptor-mediated NAD was unaffected by the Cl- channel Tyrosine Kinase Inhibitor Library blockers, 9-anthracene carboxylic acid (100 mu M) and niflumic acid (10 mu M) or by the nonselective cation channel blocker, SKF 96365 (10 mu M). These findings indicate that the NAD is produced by activation of both alpha(1)- and alpha(2)-adrenoceptors. The alpha(2)-adrenoceptor-mediated component is produced by closure of K-ATP channels whereas the alpha(1)-adrenoceptor-mediated component is most likely mediated by closure of another type of K+ channel. (C) 2010 Elsevier BM. All rights reserved.”
“The aim of this study was to compare the prevalence of diagnosed neurodevelopmental disorders in children exposed, in utero, to different antiepileptic drug treatments.