In the fifth generation communication system, millimeter wave (mmWave) networks will coexist with traditional micro wave (μWave) networks, which allows for higher data transmission rate and better user experience. In this paper, we give a comprehensive framework of mathematical models and analytical methods for multi-tier mmWave and μWave hybrid caching networks based on stochastic geometry. We propose an association strategy by assuming average biased-received power association and Rayleigh fading. Accordingly, by using a D-ball approximating blockage model of mmWave networks, expressions of the cell association probability and the coverage probability of the hybrid networks are derived. Also, we use the average successful delivery probability as the performance metric to analyze the existing caching placement strategies. Simulation results validate the accuracy of our analytical conclusions.

Cooperative Non-Orthogonal Multiple Access (NOMA) with Simultaneous Wireless Information and Power Transfer (SWIPT) communication can effectively improve the spectrum efficiency and energy efficiency of the wireless networks with extend coverage. An important design issue is to incentivize a relaying center user to participate in the cooperative process and achieve a win-win situation to both the BS and the center user. Some private information of the center users are hidden from the BS in the networks. We apply a contract theory-based incentive mechanism under such asymmetric information scenario to incentives center user to join the cooperative communication to maximize the BS profit utility and to guarantee the center user’s expect payoff. A match theory-based Gale-Shapley algorithm is proposed to obtain the optimal strategy with low computation complexity. Simulation results indicated the network performance of our proposed cooperative transmission is much better than the conventional NOMA transmission and the benefit utility of the BS with the stable match strategy is nearly close to the complete channel state information multi-users scenario while the center users get the satisfied expect payoffs.

Rationale: The 14-3-3 protein family is known to interact with many proteins in non-cardiac cell types to regulate multiple signaling pathways, particularly those relating to energy and protein homeostasis; and the 14-3-3 network is a therapeutic target of critical metabolic and proteostatic signaling in cancer and neurological diseases. Although the heart is critically sensitive to nutrient and energy alterations, and multiple signaling pathways coordinate to maintain the cardiac cell homeostasis, neither the structure of cardiac 14-3-3 protein interactome, nor potential functional roles of 14-3-3 protein-protein interactions (PPIs) in heart has been explored. Objective: To establish the comprehensive landscape and characterize the functional role of cardiac 14-3-3 PPIs. Methods and Results: We evaluated both RNA expression and protein abundance of 14-3-3 isoforms in mouse heart, followed by co-immunoprecipitation of 14-3-3 proteins and mass spectrometry in left ventricle. We identified 52 proteins comprising the cardiac 14-3-3 interactome. Multiple bioinformatic analyses indicated that more than half of the proteins bound to 14-3-3 are related to mitochondria; and the deduced functions of the mitochondrial 14-3-3 network are to regulate cardiac ATP production via interactions with mitochondrial inner membrane proteins, especially those in mitochondrial complex I. Binding to ribosomal proteins, 14-3-3 proteins likely coordinate protein synthesis and protein quality control. Localizations of 14-3-3 proteins to mitochondria and ribosome were validated via immunofluorescence assays. The deduced function of cardiac 14-3-3 PPIs is to regulate cardiac metabolic homeostasis and proteostasis. Conclusions: Thus, the cardiac 14-3-3 interactome may be a potential therapeutic target in cardiovascular metabolic and proteostatic disease states, as it already is in cancer therapy.