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Small cell deployment offers a low-cost solution for the boosted traffic demand in heterogeneous cellular networks (HCNs). Besides improved spatial spectrum efficiency and energy efficiency, future HCNs are also featured with the trend of network architecture convergence and feasibility for flexible mobile applications. To achieve these goals, dual connectivity (DC) is playing a more and more important role to support control/user-plane splitting, which enables maintaining fixed control channel connections for reliability. In this paper, we develop a tractable framework for the downlink SINR analysis of DC assisted HCN. Based on stochastic geometry model, the data-control joint coverage probabilities under multi-frequency and single-frequency tiering are derived, which involve quick integrals and admit simple closed-forms in special cases. Monte Carlo simulations confirm the accuracy of the expressions. It is observed that the increase in mobility robustness of DC is at the price of control channel SINR degradation. This degradation severely worsens the joint coverage performance under single-frequency tiering, proving multi-frequency tiering a more feasible networking scheme to utilize the advantage of DC effectively. Moreover, the joint coverage probability can be maximized by adjusting the density ratio of small cell and macro cell eNBs under multi-frequency tiering, though changing cell association bias has little impact on the level of the maximal coverage performance. [ABSTRACT FROM AUTHOR]

Background and objective T peptide is extensively used in anti-tumor treatment. The aims of this study were to investigate whether T peptide enhances cisplatinum efficiency while reducing its side effects and to identify its effective mechanisms. Methods (1) Human macrophage U937 cells were treated with T peptide and/or cisplatinum. The levels of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) of each group were detected by enzyme-linked immunosorbent assay (ELISA); (2) Xenograft mouse models of human lung cancer were treated with T peptide and/or cisplatinum once every five days for three times. Tumor volumes were measured during treatment; (3) The percentages of macrophages in the peripheral blood of the xenograft mouse models were measured by FACS. Results (1) Compared with other groups, the level of TNF-α was significantly higher in the human macrophage U937 cells that were treated with T peptide combined with cisplatinum. The levels of IFN-γ were significantly higher in human macrophage U937 cells that were treated with T peptide alone or T peptide combined with cisplatinum; (2) In the xenograft mouse models, T peptide combined with cisplatinum treatment significantly inhibited tumor growth without weight loss compared with the other groups; (3) The percentages of macrophages in the peripheral blood were significantly higher in the xenograft mouse models that were treated with T peptide combined with cisplatinum compared with in the other groups. Conclusion T peptide promotes macrophage proliferation and increases tumor cell killing factors (TNF-α, IFN-γ) in vitro. Moreover, T peptide enhances the efficacy of cisplatin and reduces its toxicity in vivo. [ABSTRACT FROM AUTHOR]