Controlled mobility in stochastic and dynamic wireless networks

We consider the use of controlled mobility in wireless networks where messages arriving randomly in time and space are collected by mobile receivers (collectors). The collectors are responsible for receiving these messages via wireless transmission by dynamically adjusting their position in the network. Our goal is to utilize a combination of wireless transmission and controlled mobility to improve the throughput and delay performance in such networks. First, we consider a system with a single collector. We show that the necessary and sufficient stability condition for such a system is given by ρ<1 where ρ is the expected system load. We derive lower bounds for the expected message waiting time in the system and develop policies that are stable for all loads ρ<1 and have asymptotically optimal delay scaling. We show that the combination of mobility and wireless transmission results in a delay scaling of Θ([1 over 1−ρ]) with the system load ρ, in contrast to the Θ([1 over (1−ρ)[superscript 2]]) delay scaling in the corresponding system without wireless transmission, where the collector visits each message location. Next, we consider the system with multiple collectors. In the case where simultaneous transmissions to different collectors do not interfere with each other, we show that both the stability condition and the delay scaling extend from the single collector case. In the case where simultaneous transmissions to different collectors interfere with each other, we characterize the stability region of the system and show that a frame-based version of the well-known Max-Weight policy stabilizes the system asymptotically in the frame length.National Science Foundation (U.S.) (Grant CNS-0915988)United States. Army Research Office. Multidisciplinary University Research Initiative (Grant W911NF-08-1-0238

The semantic priming project

10.3758/s13428-012-0304-zBehavior Research Methods4541099-111

The RET/PTC3 oncogene activates classical NF-[kappa]B by stabilizing NIK

The oncogenic fusion protein RET/PTC3 (RP3) that is expressed in papillary thyroid carcinoma (PTC) and thyroid epithelia in Hashimoto's thyroiditis activates nuclear factor-kappa B (NF-[kappa]B) and induces pro-inflammatory gene expression; however, the mechanism of this activation is unknown. To address this, we expressed RP3 in murine embryonic fibroblasts (MEFs) lacking key classical and noncanonical NF-[kappa]B signaling components. In wild-type MEFs, RP3 upregulated CCL2, CXCL1, granulocyte-macrophage colony-stimulating factor and tumor necrosis factor expression and activated classical but not noncanonical NF-[kappa]B. RP3-activated NF-[kappa]B-in I[kappa]B kinase (IKK)[beta].sup.-/-] MEFs but not IKK[alpha]- or NF-[kappa]B essential modulator (NEMO)-deficient cells and activation was inhibited by a peptide that blocks NEMO binding to the IKKs. RP3 increased the levels of NF-[kappa]B-inducing kinase (NIK) and did not activate NF-[kappa]B in NIK-deficient MEFs. Notably, NIK stabilization was not accompanied by TRAF3 degradation demonstrating that RP3 disrupts normal basal NIK regulation. Dominant-negative NIK blocked RP3-induced NF-[kappa]B activation and an RP3 signaling mutant ([RP3.SUP.Y588F]) did not stabilize NIK. Finally, examination of PTC specimens revealed strong positive staining for NIK. We therefore conclude that RP3 activates classical NF-[kappa]B via NIK, NEMO and IKK[alpha]. Importantly, our findings reveal a novel mechanism for oncogene-induced NF-[kappa]B activation via stabilization of NIK. Oncogene (2011) 30, 87-96; doi: 10.1038/onc.2010.396; published online 6 September 2010 Keywords: Hashimoto's thyroiditis; IKK; NIK; NF-[kappa]B; RET/PTC; thyroid cancerAcademi