31,845 research outputs found

    A signaling protocol for service function localization

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    Current proposals for chaining service functions (SFs) do not address some critical management issues, such as the discovery of SF instances close to IP data paths. This information is crucial for deploying complex services both in large cloud networks, where SFs may be moved or replicated, and in the emerging fog/mobile edge computing systems. For this purpose, in this letter, we propose the distributed off-path signaling protocol. We show the protocol functions and demonstrate its scalability and effectiveness by experimental results

    Differences in localization of P2X7 during epithelial wound healing in pre-type II diabetic models

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    Corneal injury, accompanied by improper wound repair, is the 4th highest cause of preventable blindness according to the World Health Organization. The cornea, which is the most densely innervated structure in the human body, serves to protect the delicate internal environment of the eye from damage. The integrity of this intricate nerve structure is critical in our ability to sense even the slightest insult to the corneal surface, with reduced sensitivity leading to increased susceptibility to trauma. In diabetes, decreased corneal sensitivity secondary to diabetic peripheral neuropathy can lead to increased corneal abrasion, ulceration, and even blindness. The P2X7 purinoreceptor is an ion channel that is expressed by the epithelium along with the intra-epithelial nerves and stromal nerves. The goal of our study was to use a type 2 diabetic mouse model (DIO) to characterize the changes in P2X7 localization and potentially correlate our results with changes in trafficking and sensory nerve loss. We hypothesized that the P2X7 receptor acts to sense changes at the leading edge and this fine tuned regulation is altered during the diabetic disease state. Further understanding of the corneal changes that occur in diabetes can help us better monitor progression of diabetic complications as well as develop new therapeutics for the treatment of diabetic corneal dysfunction

    Fast Cell Discovery in mm-wave 5G Networks with Context Information

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    The exploitation of mm-wave bands is one of the key-enabler for 5G mobile radio networks. However, the introduction of mm-wave technologies in cellular networks is not straightforward due to harsh propagation conditions that limit the mm-wave access availability. Mm-wave technologies require high-gain antenna systems to compensate for high path loss and limited power. As a consequence, directional transmissions must be used for cell discovery and synchronization processes: this can lead to a non-negligible access delay caused by the exploration of the cell area with multiple transmissions along different directions. The integration of mm-wave technologies and conventional wireless access networks with the objective of speeding up the cell search process requires new 5G network architectural solutions. Such architectures introduce a functional split between C-plane and U-plane, thereby guaranteeing the availability of a reliable signaling channel through conventional wireless technologies that provides the opportunity to collect useful context information from the network edge. In this article, we leverage the context information related to user positions to improve the directional cell discovery process. We investigate fundamental trade-offs of this process and the effects of the context information accuracy on the overall system performance. We also cope with obstacle obstructions in the cell area and propose an approach based on a geo-located context database where information gathered over time is stored to guide future searches. Analytic models and numerical results are provided to validate proposed strategies.Comment: 14 pages, submitted to IEEE Transaction on Mobile Computin

    Context Information for Fast Cell Discovery in mm-wave 5G Networks

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    The exploitation of the mm-wave bands is one of the most promising solutions for 5G mobile radio networks. However, the use of mm-wave technologies in cellular networks is not straightforward due to mm-wave harsh propagation conditions that limit access availability. In order to overcome this obstacle, hybrid network architectures are being considered where mm-wave small cells can exploit an overlay coverage layer based on legacy technology. The additional mm-wave layer can also take advantage of a functional split between control and user plane, that allows to delegate most of the signaling functions to legacy base stations and to gather context information from users for resource optimization. However, mm-wave technology requires high gain antenna systems to compensate for high path loss and limited power, e.g., through the use of multiple antennas for high directivity. Directional transmissions must be also used for the cell discovery and synchronization process, and this can lead to a non-negligible delay due to the need to scan the cell area with multiple transmissions at different directions. In this paper, we propose to exploit the context information related to user position, provided by the separated control plane, to improve the cell discovery procedure and minimize delay. We investigate the fundamental trade-offs of the cell discovery process with directional antennas and the effects of the context information accuracy on its performance. Numerical results are provided to validate our observations.Comment: 6 pages, 8 figures, in Proceedings of European Wireless 201

    Identity and Function of a Cardiac Mitochondrial Small Conductance Ca2+-Activated K+ Channel Splice Variant

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    We provide evidence for location and function of a small conductance, Ca2+-activated K+ (SKCa) channel isoform 3 (SK3) in mitochondria (m) of guinea pig, rat and human ventricular myocytes. SKCa agonists protected isolated hearts and mitochondria against ischemia/reperfusion (IR) injury; SKCa antagonists worsened IR injury. Intravenous infusion of a SKCa channel agonist/antagonist, respectively, in intact rats was effective in reducing/enhancing regional infarct size induced by coronary artery occlusion. Localization of SK3 in mitochondria was evidenced by Western blot of inner mitochondrial membrane, immunocytochemical staining of cardiomyocytes, and immunogold labeling of isolated mitochondria. We identified a SK3 splice variant in guinea pig (SK3.1, aka SK3a) and human ventricular cells (SK3.2) by amplifying mRNA, and show mitochondrial expression in mouse atrial tumor cells (HL-1) by transfection with full length and truncated SK3.1 protein. We found that the N-terminus is not required for mitochondrial trafficking but the C-terminus beyond the Ca2+ calmodulin binding domain is required for Ca2+ sensing to induce mK+ influx and/or promote mitochondrial localization. In isolated guinea pig mitochondria and in SK3 overexpressed HL-1 cells, mK+ influx was driven by adding CaCl2. Moreover, there was a greater fall in membrane potential (ΔΨm), and enhanced cell death with simulated cell injury after silencing SK3.1 with siRNA. Although SKCa channel opening protects the heart and mitochondria against IR injury, the mechanism for favorable bioenergetics effects resulting from SKCa channel opening remains unclear. SKCa channels could play an essential role in restraining cardiac mitochondria from inducing oxidative stress-induced injury resulting from mCa2+ overload
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