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Ultra‐dense small cell networks (UD‐SCNs) have been identified as a promising scheme for next‐generation wireless networks capable of meeting the ever‐increasing demand for higher transmission rates and better quality of service. However, UD‐SCNs will inevitably suffer from severe interference among the small cell base stations, which will lower their spectral efficiency. In this paper, we propose a software‐defined networking (SDN)‐based hierarchical agglomerative clustering (SDN‐HAC) framework, which leverages SDN to centrally control all sub‐channels in the network, and decides on cluster merging using a similarity criterion based on a suitability function. We evaluate the proposed algorithm through simulation. The obtained results show that the proposed algorithm performs well and improves system payoff by 18.19% and 436.34% when compared with the traditional network architecture algorithms and non‐cooperative scenarios, respectively.
We studied the influence of silica and glass fibers on the properties of polyester non-woven padding, fixing interesting changes in thermoinsulation, thickness and stiffness of obtained composites. It was found that the combination of inorganic and polyester fibers allowed for obtaining improved thermoinsulating property, compared to non-woven materials based on individual fibers. The improvement is attributed to the enhanced reflectance and the decreased air permeability, which can reduce the heat lost through radiation and convection. The application of inorganic fibers also made the development of non-woven materials with small thickness, keeping thermoinsulating property similar or better, compared to the commonly used polyester non-woven padding. Furthermore, the designed non-woven composites in real models of winter jackets were evaluated in a climate chamber at -10 oC by infrared thermal camera. The results showed that the addition of inorganic fibers allowed the surface temperature of winter jackets more than 5 oC lower than that of winter jacket with pure polyester padding. They significantly enhanced the protection from cold and reduced heat loss from the human body.
Due to the high toxicity of lead ions (Pb2+) and volatile organic compounds (VOCs) to human health and the environment, increasing attention has been paid by scientists to the development of simple, flexible and sensitive sensors or methods that are capable of tracing Pb2+ ions or VOCs with colorimetric visualization. In this study, the fabrication of colorimetric sensors based on histidine-functionalized diacetylene (His-DA), chromatic π-conjugated liposomes, for tracing Pb2+ ions was described. With a suitable molar ratio (4:1) between the10,12-pentacosadiynoic acid (PCDA) and His-DA monomers, the histidine units of the hybrid liposomes could rationally interrupt the efficient backbone length of polydiacetylene (PDA) chains, which causes the probe to be highly sensitive and selective for colorimetric visualization of tracing Pb2+ ions. Moreover, the His-PDA films also displayed sensitivity to volatile organic solvents or vapors, which could promote vivid color changes from blue to purple or pink. These interesting findings indicate that histidine-functionalized diacetylene may offer a promising way to design smart devices for real applications of sensing or tracing hazardous substances in the future.
Purpose: Neonatal hypoxic ischemic encephalopathy (HIE) is an essential factor underlying neonatal death and disability. Thisstudy sought to explore the role of miR-146b-5p in regulating neonatal HIE. Materials and Methods: In vitro and in vivo HIE models were established in PC12 cells and 10-day neonatal Sprague Dawley rats,respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to assess miR-146b-5p expressionand inflammatory factors [interleukin (IL)-6 and tumor necrosis factor (TNF)-α] in brain lesions and PC12 cells, while enzymelinkedimmunosorbent assay was employed to detect the expression of oxidative stress factors (SOD and GSH-Px). Gain- andloss-assays of miR-146b-5p were conducted to verify its role in modulating the viability and apoptosis of PC12 cells under oxygenglucosedeprivation (OGD) treatment. Expression of TLR4, IRAK1, TRAF6, TAK1, and NF-κB were examined by qRT-PCR and/orWestern blot. Dual luciferase activity assay was conducted to identify relationships between miR-146b-5p and IRAK1. Results: In the HIE models, significant oxidative stress and inflammatory responses emerged upon upregulation of TLR4/IRAK1/TRAF6/TAK1/NF-κB signaling. Overexpression of miR-146b-5p greatly inhibited OGD-induced PC12 cell injury, inflammatoryresponses, and oxidative stress. Inhibiting miR-146b-5p, however, had the opposite effects. IRAK1 was found to be a target of miR-146b-5p, and miR-146b-5p overexpression suppressed the activation of IRAK1/TRAF6/TAK1/NF-κB signaling. Conclusion: This study demonstrated that miR-146b-5p overexpression alleviates HIE-induced neuron injury by inhibiting theIRAK1/TRAF6/TAK1/NF-κB pathway.
For enhancing the coverage of wireless networks and increasing the spectrum efficiency, small cell networks (SCNs) are considered to be one of the most prospective schemes. Most of the existing literature on resource allocation among non-cooperative small cell base stations (SBSs) has widely drawn close attention and there are only a small number of the cooperative ideas in SCNs. Based on the motivation, we further investigate the cooperative approach, which is formulated as a coalition formation game with power control algorithm (CFG-PC). First, we formulate the downlink sub-channel resource allocation problem in an SCN as a coalition formation game. Pareto order and utilitarian order are applied to form coalitions respectively. Second, to achieve more availability and efficiency power assignment, we expand and solve the power control using particle swarm optimization (PSO). Finally, with our proposed algorithm, each SBS can cooperatively work and eventually converge to a stable SBS partition. As far as the transmit rate of per SBS and the system rate are concerned respectively, simulation results indicate that our proposed CFG-PC has a significant advantage, relative to a classical coalition formation algorithm and the non-cooperative case.
Cloud storage is becoming more and more popular because of its elasticity and pay-as-you-go storage service manner. In some cloud storage scenarios, the data that are stored in the cloud may be shared by a group of users. To verify the integrity of cloud data in this kind of applications, many auditing schemes for shared cloud data have been proposed. However, all of these schemes do not consider the access authorization problem for users, which makes the revoked users still able to access the shared cloud data belonging to the group. In order to deal with this problem, we propose a novel public auditing scheme for shared cloud data in this paper. Different from previous work, in our scheme, the user in a group cannot any longer access the shared cloud data belonging to this group once this user is revoked. In addition, we propose a new random masking technique to make our scheme preserve both data privacy and identity privacy. Furthermore, our scheme supports to enroll a new user in a group and revoke an old user from a group. We analyze the security of the proposed scheme and justify its performance by concrete implementations.
MicroRNAs (miRNAs) are regulatory small non-coding RNAs that can regulate gene expression by binding to gene elements, such as the gene promotor 5UTR, mainly in the 3UTR of mRNA. One miRNA targets many mRNAs, which can be regulated by many miRNAs, leading to a complex metabolic network. In our study, we found that the expression level of miR-590-5p is higher in the human hepatocellular carcinoma cell line HepG2 than in the normal hepatocellular cell line L02. Downregulation of miR-590-5p inhibited proliferation and invasion of hepatocellular carcinoma cells (HCCs). We also showed that expression of TGF-beta RII, which has been regarded as a regulator of tumor proliferation, invasion, and migration in hepatocellular carcinoma, is regulated by miRNA-590-5p. In addition, miR-590-5p downregulated the expression of TGF- beta RII by targeting the 3UTR of mRNA. We also found that downregulation of miR-590-5p was associated with an elevation of TGF-beta RII and inhibition of proliferation and invasion in HepG2 cells. Furthermore, overex-pression of miR-590-5p was associated with upregulation of TGF-beta RII and could promote proliferation and invasion in L02 cells. In conclusion, we determined that TGF-beta RII is a novel target of miRNA-590-5p. Thus, the role of TGF-beta RII in regulating proliferation and invasion of human HCCs is controlled by miR-590-5p. In other words, miR-590-5p promotes proliferation and invasion in human HCCs by directly targeting TGF-beta RII.