This paper considers a joint optimal design of admission control and resource allocation for multimedia services delivery in high-speed railway (HSR) wireless networks. A stochastic network optimization problem is formulated which aims at maximizing the system utility while stabilizing all transmission queues under the average power constraint. By introducing virtual queues, the original problem is equivalently transformed into a queue stability problem, which can be naturally decomposed into three separate subproblems: utility maximization, admission control, and resource allocation. A threshold-based admission control strategy is proposed for the admission control subproblem. And a distributed resource allocation scheme is developed for the mixed-integer resource allocation subproblem with guaranteed global optimality. Then a dynamic admission control and resource allocation algorithm is proposed, which is suitable for distributed implementation. Finally, the performance of the proposed algorithm is evaluated by theoretical analysis and numerical simulations under realistic conditions of HSR wireless networks.

No abstract

No abstract

Background Distant metastasis is the major cause of clear cell renal cell carcinoma (ccRCC)-associated mortality. However, molecular mechanisms involved in ccRCC metastasis remain to be fully understood. With the increasing appreciation of the role of long non-coding RNAs (lncRNAs) in cancer development, progression, and treatment resistance, the list of aberrantly expressed lncRNAs contributing to ccRCC pathogenesis is expanding rapidly. Methods Bioinformatics analysis was carried out to interrogate publicly available ccRCC datasets. In situ hybridization and qRT-PCR assays were used to test lncRNA expression in human ccRCC tissues and cell lines, respectively. Chromatin immunoprecipitation and luciferase reporter assays were used to examine transcriptional regulation of gene expression. Wound healing as well as transwell migration and invasion assays were employed to monitor ccRCC cell migration and invasion in vitro. ccRCC metastasis was also examined using mouse models in vivo. RNA pulldown and RNA immunoprecipitation were performed to test RNA–protein associations, whereas RNA-RNA interactions were tested using domain-specific chromatin isolation by RNA purification. Results MILIP expression was upregulated in metastatic compared with primary ccRCC tissues. The increased MILIP expression in metastatic ccRCC cells was driven by the transcription factor AP-2 gamma (TFAP2C). Knockdown of MILIP diminished the potential of ccRCC cell migration and invasion in vitro and reduced the formation of ccRCC metastatic lesions in vivo. The effect of MILIP on ccRCC cells was associated with alterations in the expression of epithelial-to-mesenchymal transition (EMT) hallmark genes. Mechanistically, MILIP formed an RNA-RNA duplex with the snail family transcriptional repressor 1 (Snai1) mRNA and bound to Y-box binding protein 1 (YBX1). This promoted the association between the YBX1 protein and the Snai1 mRNA, leading to increased translation of the latter. Snai1 in turn played an important role in MILIP-driven ccRCC metastasis. Conclusions The TFAP2C-responsive lncRNA MILIP drives ccRCC metastasis. Targeting MILIP may thus represent a potential avenue for ccRCC treatment.