A Novel Cross-Layer Authentication Protocol for the Internet of Things

An innovative cross-layer authentication protocol that integrates cryptography-based authentication and physical layer authentication (PLA) is proposed for massive cellular Internet of things (IoT) systems. Due to dramatic increases in the number of cellular IoT devices, a centralized authentication architecture in which a mobility management entity in core networks administers authentication of massive numbers of IoT devices may cause network congestion with large signaling overhead. Thus, a distributed authentication architecture in which a base station in radio access networks authenticates IoT devices locally is presented. In addition, a cross-layer authentication protocol is designed with a novel integration strategy under the distributed authentication architecture, where PLA, which employs physical features for authentication, is used as preemptive authentication in the proposed protocol. Theoretical analysis and numerical simulations were performed to analyze the trade-off between authentication performance and overhead in the proposed authentication method compared with existing authentication protocols. The results demonstrate that the proposed protocol outperforms conventional authentication and key agreement protocols in terms of overhead and computational complexity while guaranteeing low authentication error probability

The impact of UK household overconfidence in public information on house prices

We investigate if house prices are affected by overconfidence of households who predict house prices using imperfect public information about economic outlook. For this purpose, we develop a new measure of household overconfidence in the Bayesian framework. For the three variables we test – changes in consumption, stock returns, and changes in human capital, we find that UK households were overconfident about the signals of consumption regardless of regions. However, households in London were overconfident about the signals of stock markets whereas those remote from London were overconfident about the signals of human capital. The results of household overconfidence appear positive in the UK housing market for our sample period from 1980 to 2018, in particular, 0.5% per quarter in London

Rewiring of PDZ Domain-Ligand Interaction Network Contributed to Eukaryotic Evolution

PDZ domain-mediated interactions have greatly expanded during metazoan evolution, becoming important for controlling signal flow via the assembly of multiple signaling components. The evolutionary history of PDZ domain-mediated interactions has never been explored at the molecular level. It is of great interest to understand how PDZ domain-ligand interactions emerged and how they become rewired during evolution. Here, we constructed the first human PDZ domain-ligand interaction network (PDZNet) together with binding motif sequences and interaction strengths of ligands. PDZNet includes 1,213 interactions between 97 human PDZ proteins and 591 ligands that connect most PDZ protein-mediated interactions (98%) in a large single network via shared ligands. We examined the rewiring of PDZ domain-ligand interactions throughout eukaryotic evolution by tracing changes in the C-terminal binding motif sequences of the PDZ ligands. We found that interaction rewiring by sequence mutation frequently occurred throughout evolution, largely contributing to the growth of PDZNet. The rewiring of PDZ domain-ligand interactions provided an effective means of functional innovations in nervous system development. Our findings provide empirical evidence for a network evolution model that highlights the rewiring of interactions as a mechanism for the development of new protein functions. PDZNet will be a valuable resource to further characterize the organization of the PDZ domain-mediated signaling proteome

Analysis of the Penn Korean Universal Dependency Treebank (PKT-UD): Manual Revision to Build Robust Parsing Model in Korean

In this paper, we first open on important issues regarding the Penn Korean Universal Treebank (PKT-UD) and address these issues by revising the entire corpus manually with the aim of producing cleaner UD annotations that are more faithful to Korean grammar. For compatibility to the rest of UD corpora, we follow the UDv2 guidelines, and extensively revise the part-of-speech tags and the dependency relations to reflect morphological features and flexible word-order aspects in Korean. The original and the revised versions of PKT-UD are experimented with transformer-based parsing models using biaffine attention. The parsing model trained on the revised corpus shows a significant improvement of 3.0% in labeled attachment score over the model trained on the previous corpus. Our error analysis demonstrates that this revision allows the parsing model to learn relations more robustly, reducing several critical errors that used to be made by the previous model.Comment: Accepted by The 16th International Conference on Parsing Technologies, IWPT 202

Beclin 1 functions as a negative modulator of MLKL oligomerisation by integrating into the necrosome complex

Necroptosis is a form of regulated cell death caused by formation of the necrosome complex. However, the factors modulating this process and the systemic pathophysiological effects of necroptosis are yet to be understood. Here, we identified that Beclin 1 functions as an anti-necroptosis factor by being recruited into the necrosome complex upon treatment with TNF alpha, Smac mimetic, and pan-caspase inhibitor and by repressing MLKL oligomerisation, thus preventing the disruption of the plasma membrane. Cells ablated or knocked-out for Beclin 1 become sensitised to necroptosis in an autophagy-independent manner without affecting the necrosome formation itself. Interestingly, the recruitment of Beclin 1 into the necrosome complex is dependent on the activation and phosphorylation of MLKL. Biochemically, the coiled-coil domain (CCD) of Beclin 1 binds to the CCD of MLKL, which restrains the oligomerisation of phosphorylated MLKL. Finally, Beclin 1 depletion was found to promote necroptosis in leukaemia cells and enhance regression of xenografted-tumour upon treatment with Smac mimetics and caspase inhibitors. These results suggest that Beclin 1 functions as a negative regulator in the execution of necroptosis by suppressing MLKL oligomerisation