13,283 research outputs found

    An Invariant Dual-beam Snowflake Antenna for Future 5G Communications

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    A broadband snowflake antenna for future 5G and millimeter-wave communications is presented. The proposed antenna has a size of 8 × 5 mm 2 . The antenna consists of a central hexagon surrounded by a series of symmetrically placed smaller hexagons around it, resulting in broadband characteristics. The impedance bandwidth of the proposed antenna ranges from 25.284-29.252 GHz. The antenna has a gain of 3.12 dBi at 28 GHz and is more than 98% efficient. A distinct feature of the proposed antenna is its dual-beam radiation pattern. The two beams remain fixed at ±50° even if the frequency is varied with in its operating band. The proposed antenna is modelled on thin Rogers substrate which makes it very useful for future 5G smart phones

    Development of a Reliable Multicast Protocol in Mobile Ad Hoc Networks

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    Mobile ad hoc network is a collection of mobile nodes forming dynamic and temporary network. The mobile nodes work in collaborative nature to carry out a given task. It can receive and transmit data packets without the use of any existing network infrastructure or centralized administration. Multicasting is among the pertinent issues of communication in such networks. The reliable delivery of multicast data packets needs feedback from all multicast receivers to indicate whether a retransmission is necessary. The Feedback Implosion Problem (FIP) states that reliable multicast in ad hoc networks suffers from redundant feedback packets, loss, duplication, and out-of-order delivery of data packets. To carry out this task, several reliable multicast protocols have been proposed to reduce the number of feedback packets from the receiver nodes. This is achieved by placing the responsibility to detect packet loss and initiating loss recovery timer on the receiver nodes which is complemented by feedback suppression. The initiating loss recovery timer depends on the number of hops between the nodes. As the dynamic nature of the number of hops between the nodes in ad hoc networks is unstable the loss recovery timer become inaccurate. Thus, the inaccuracy of the loss recovery timer, in return, causes extra overhead and more delays. The main objectives of this research are to enhance the FIP and decrease the recovery delays in reliable multicast protocol for mobile ad hoc networks using suggested approaches. First, the Source Tree Reliable Multicast (STRM) protocol adopting a novel technique to select a subset of one-hop neighbors from the sender node as its Forward Servers (FS). The key idea behind selecting this subset one-hop neighbors is to forward the retransmitted lost data packets and to receive the feedback packets from the receiver nodes. Second, proposed two algorithms to improve the performance of the STRM protocol. The first algorithm is developed to avoid the buffer overflow in the FS nodes. This is achieved by managing the buffer of the FS nodes; by selecting the FS nodes depending on the empty buffer size it has and reducing the amount of feedback sent from the receiver nodes to their FS node. The second algorithm is developed to decrease the number of duplicated packets in the multicast members in the local group. This is achieved by sending the repair packets only to the member that has requested it. The FS in the local group should create a dynamic and temporary sub group whose members are only the members that requested the retransmission of the repair packet. The approaches were tested using detailed discrete-event simulation model which was developed encompassing messaging system that includes error, delay and mobility models to characterize the performance benefits of the proposed algorithms in comparison to ReMHoc protocol. Our approaches achieve up to 2.19% improvement on average packet delivery ratio, 3.3% on requested packets, and 46% on recovery latency time without incurring any additional communication or intense computation

    Receptor and secreted targets of Wnt-1/beta-catenin signalling in mouse mammary epithelial cells.

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    BackgroundDeregulation of the Wnt/ beta-catenin signal transduction pathway has been implicated in the pathogenesis of tumours in the mammary gland, colon and other tissues. Mutations in components of this pathway result in beta-catenin stabilization and accumulation, and the aberrant modulation of beta-catenin/TCF target genes. Such alterations in the cellular transcriptional profile are believed to underlie the pathogenesis of these cancers. We have sought to identify novel target genes of this pathway in mouse mammary epithelial cells.MethodsGene expression microarray analysis of mouse mammary epithelial cells inducibly expressing a constitutively active mutant of beta-catenin was used to identify target genes of this pathway.ResultsThe differential expression in response to DeltaNbeta-catenin for five putative target genes, Autotaxin, Extracellular Matrix Protein 1 (Ecm1), CD14, Hypoxia-inducible gene 2 (Hig2) and Receptor Activity Modifying Protein 3 (RAMP3), was independently validated by northern blotting. Each of these genes encodes either a receptor or a secreted protein, modulation of which may underlie the interactions between Wnt/beta-catenin tumour cells and between the tumour and its microenvironment. One of these genes, Hig2, previously shown to be induced by both hypoxia and glucose deprivation in human cervical carcinoma cells, was strongly repressed upon DeltaNbeta-catenin induction. The predicted N-terminus of Hig2 contains a putative signal peptide suggesting it might be secreted. Consistent with this, a Hig2-EGFP fusion protein was able to enter the secretory pathway and was detected in conditioned medium. Mutation of critical residues in the putative signal sequence abolished its secretion. The expression of human HIG2 was examined in a panel of human tumours and was found to be significantly downregulated in kidney tumours compared to normal adjacent tissue.ConclusionsHIG2 represents a novel non-cell autonomous target of the Wnt pathway which is potentially involved in human cancer
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