Effective Capacity in Broadcast Channels with Arbitrary Inputs

We consider a broadcast scenario where one transmitter communicates with two receivers under quality-of-service constraints. The transmitter initially employs superposition coding strategies with arbitrarily distributed signals and sends data to both receivers. Regarding the channel state conditions, the receivers perform successive interference cancellation to decode their own data. We express the effective capacity region that provides the maximum allowable sustainable data arrival rate region at the transmitter buffer or buffers. Given an average transmission power limit, we provide a two-step approach to obtain the optimal power allocation policies that maximize the effective capacity region. Then, we characterize the optimal decoding regions at the receivers in the space spanned by the channel fading power values. We finally substantiate our results with numerical presentations.Comment: This paper will appear in 14th International Conference on Wired&Wireless Internet Communications (WWIC

TBK1 mutation spectrum in an extended European patient cohort with frontotemporal dementia and amyotrophic lateral sclerosis

We investigated the mutation spectrum of the TANK-Binding Kinase 1 (TBK1) gene and its associated phenotypic spectrum by exonic resequencing of TBK1 in a cohort of 2,538 patients with frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), or FTD plus ALS, ascertained within the European Early-Onset Dementia Consortium. We assessed pathogenicity of predicted protein-truncating mutations by measuring loss of RNA expression. Functional effect of in-frame amino acid deletions and missense mutations was further explored in vivo on protein level and in vitro by an NFκB-induced luciferase reporter assay and measuring phosphorylated TBK1. The protein-truncating mutations led to the loss of transcript through nonsense-mediated mRNA decay. For the in-frame amino acid deletions, we demonstrated loss of TBK1 or phosphorylated TBK1 protein. An important fraction of the missense mutations compromised NFκB activation indicating that at least some functions of TBK1 are lost. Although missense mutations were also present in controls, over three times more mutations affecting TBK1 functioning were found in the mutation fraction observed in patients only, suggesting high-risk alleles (P = 0.03). Total mutation frequency for confirmed TBK1 LoF mutations in the European cohort was 0.7%, with frequencies in the clinical subgroups of 0.4% in FTD, 1.3% in ALS, and 3.6% in FTD-ALS