Cellular Offloading via Downlink Cache Placement

In this paper, the downlink file transmission within a finite lifetime is optimized with the assistance of wireless cache nodes. Specifically, the number of requests within the lifetime of one file is modeled as a Poisson point process. The base station multicasts files to downlink users and the selected the cache nodes, so that the cache nodes can help to forward the files in the next file request. Thus we formulate the downlink transmission as a Markov decision process with random number of stages, where transmission power and time on each transmission are the control policy. Due to random number of file transmissions, we first proposed a revised Bellman's equation, where the optimal control policy can be derived. In order to address the prohibitively huge state space, we also introduce a low-complexity sub-optimal solution based on an linear approximation of the value function. The approximated value function can be calculated analytically, so that conventional numerical value iteration can be eliminated. Moreover, the gap between the approximated value function and the real value function is bounded analytically. It is shown by simulation that, with the approximated MDP approach, the proposed algorithm can significantly reduce the resource consumption at the base station.Comment: Submitted for IEEE ICC 201

GDoF of Interference Channel with Limited Cooperation under Finite Precision CSIT

The Generalized Degrees of Freedom (GDoF) of the two user interference channel are characterized for all parameter regimes under the assumption of finite precision channel state information at the transmitters (CSIT), when a limited amount of cooperation is allowed between the transmitters in the form of π DoF of shared messages. In all cases, the number of over- the-air bits that each cooperation bit buys is shown to be equal to either 0, 1, 1/2 or 1/3

GDoF of Interference Channel with Limited Cooperation under Finite Precision CSIT

The Generalized Degrees of Freedom (GDoF) of the two user interference channel are characterized for all parameter regimes under the assumption of finite precision channel state information at the transmitters (CSIT), when a limited amount of cooperation is allowed between the transmitters in the form of π DoF of shared messages. In all cases, the number of over- the-air bits that each cooperation bit buys is shown to be equal to either 0, 1, 1/2 or 1/3

Progress and Perspective of CRISPR‐Cas9 Technology in Translational Medicine

Abstract Translational medicine aims to improve human health by exploring potential treatment methods developed during basic scientific research and applying them to the treatment of patients in clinical settings. The advanced perceptions of gene functions have remarkably revolutionized clinical treatment strategies for target agents. However, the progress in gene editing therapy has been hindered due to the severe off‐target effects and limited editing sites. Fortunately, the development in the clustered regularly interspaced short palindromic repeats associated protein 9 (CRISPR‐Cas9) system has renewed hope for gene therapy field. The CRISPR‐Cas9 system can fulfill various simple or complex purposes, including gene knockout, knock‐in, activation, interference, base editing, and sequence detection. Accordingly, the CRISPR‐Cas9 system is adaptable to translational medicine, which calls for the alteration of genomic sequences. This review aims to present the latest CRISPR‐Cas9 technology achievements and prospect to translational medicine advances. The principle and characterization of the CRISPR‐Cas9 system are firstly introduced. The authors then focus on recent pre‐clinical and clinical research directions, including the construction of disease models, disease‐related gene screening and regulation, and disease treatment and diagnosis for multiple refractory diseases. Finally, some clinical challenges including off‐target effects, in vivo vectors, and ethical problems, and future perspective are also discussed

SALL4 correlates with proliferation, metastasis, and poor prognosis in prostate cancer by affecting MAPK pathway

Abstract Background The mechanism involved in prostate cancer (PCa) metastasis is still poorly understood, and several oncogenes are known to regulate this process. However, the role of spalt‐like transcription factor 4 (SALL4) in PCa metastasis remains unclear. Methods We performed RNA‐sequencing to compare the mRNA expression profiles of seven localized PCa tissues and six metastatic PCa tissues. SALL4 was then identified and compared in the localized PCa and metastatic PCa. Immunohistochemical studies, qRT‐PCR, and Western blot were performed to analyze the expression of SALL4 in PCa patients and cell lines. SALL4 expression and its relevance to clinical traits and prognosis were further explored in the TCGA database and in our 68 clinical samples. Subsequently, we knocked down SALL4 in DU145 and PC3 cells and performed a series of functional assays to explore the effect of SALL4 on PCa progression. Finally, protein levels of SALL4 and core components of the MAPK pathway were measured by Western blot, and cells were treated with PD0325901 to observe proliferation and metastasis. Results Significantly higher expression of SALL4 was found in metastatic PCa than in localized PCa. In addition, high SALL4 expression was significantly associated with high pathological T stage, N stage, Gleason score, and poor disease‐free survival in TCGA database and in our clinical samples. Functional studies indicated that knockdown of SALL4 in DU145 and PC3 inhibited proliferation, migration, and angiogenesis. Furthermore, the ERK and P38 protein phosphorylation significantly reduced after knockdown of SALL4 in DU145 and PC3, indicating the inactivation of the MAPK signaling pathway. Finally, the proliferation and migration ability of DU145 and PC3 cells were significantly decreased after PD0325901 treatment. Conclusions SALL4 predicts unfavorable outcome and is closely associated with PCa progression, suggesting that SALL4 may be a promising prognostic marker and potential therapeutic target for PCa