879 resultados para Uniquely ergodic


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Active network scanning injects traffic into a network and observes responses to draw conclusions about the network. Passive network analysis works by looking at network meta data or by analyzing traffic as it traverses a fixed point on the network. It may be infeasible or inappropriate to scan critical infrastructure networks. Techniques exist to uniquely map assets without resorting to active scanning. In many cases, it is possible to characterize and identify network nodes by passively analyzing traffic flows. These techniques are considered in particular with respect to their application to power industry critical infrastructure.

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We present the Pan-STARRS1 discovery and light curves, and follow-up MMT and Gemini spectroscopy of an ultraluminous supernova (ULSN; dubbed PS1-11bam) at a redshift of z = 1.566 with a peak brightness of M UV ≈ -22.3 mag. PS1-11bam is one of the highest redshift spectroscopically confirmed SNe known to date. The spectrum exhibits broad absorption features typical of previous ULSNe (e.g., C II, Si III), and strong and narrow Mg II and Fe II absorption lines from the interstellar medium (ISM) of the host galaxy, confirmed by an [O II]λ3727 emission line at the same redshift. The equivalent widths of the Fe II λ2600 and Mg II λ2803 lines are in the top quartile of the quasar intervening absorption system distribution, but are weaker than those of gamma-ray burst intrinsic absorbers (i.e., GRB host galaxies). We also detect the host galaxy in pre-explosion Pan-STARRS1 data and find that its UV spectral energy distribution is best fit with a young stellar population age of τ* ≈ 15-45 Myr and a stellar mass of M * ≈ (1.1-2.6) × 109 M ⊙ (for Z = 0.05-1 Z ⊙). The star formation rate inferred from the UV continuum and [O II]λ3727 emission line is ≈10 M ⊙ yr-1, higher than in previous ULSN hosts. PS1-11bam provides the first direct demonstration that ULSNe can serve as probes of the ISM in distant galaxies. The depth and red sensitivity of PS1 are uniquely suited to finding such events at cosmologically interesting redshifts (z ~ 1-2); the future combination of LSST and 30 m class telescopes promises to extend this technique to z ~ 4.

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Cathepsin S is a member of the cysteine cathepsin protease family. It is a lysosomal protease which can promote degradation of damaged or unwanted proteins in the endo-lysosomal pathway. Additionally, it has more specific roles such as MHC class II antigen presentation, where it is important in the degradation of the invariant chain. Unsurprisingly, mis-regulation has implicated cathepsin S in a variety of pathological processes including arthritis, cancer, and cardiovascular disease, where it becomes secreted and can act on extracellular substrates. In comparison to many other cysteine cathepsin family members, cathepsin S has uniquely restricted tissue expression and is more stable at a neutral pH, which supports its involvement and importance in localised disease microenvironments. In this review, we examine the known involvement of cathepsin S in disease, particularly with respect to recent work indicating its role in mediating pain, diabetes, and cystic fibrosis. We provide an overview of current literature with regards cathepsin S as a therapeutic target, as well as its role and potential as a predictive diagnostic and/or prognostic marker in these diseases.

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Bioresorbable polymers increasingly are the materials of choice for implantable orthopaedic fixation devices. Controlled degradation of these polymers is vital for preservation of mechanical properties during tissue repair and controlled release of incorporated agents such as osteoconductive or anti-microbial additives. The work outlined in this paper investigates the use of low energy electron beam irradiation to surface modify polyhydroxyacid samples incorporating beta tricalcium phosphate (β-TCP). This work uniquely demonstrates that surface modification of bioresorbable polymers through electron beam irradiation allows for the early release of incorporated agents such as bioactive additives. Samples were e-beam irradiated at an energy of 125 keV and doses of either 150 kGy or 500 kGy. Irradiated and non-irradiated samples were degraded in phosphate buffered saline (PBS), to simulate bioresorption, followed by characterisation. The results show that low energy e-beam irradiation enhances surface hydrolytic degradation in comparison to bulk and furthermore allows for earlier release of incorporated calcium via dissolution into the surrounding medium.

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Radio-frequency (RF) impairments, which intimately exist in wireless communication systems, can severely limit the performance of multiple-input-multiple-output (MIMO) systems. Although we can resort to compensation schemes to mitigate some of these impairments, a certain amount of residual impairments always persists. In this paper, we consider a training-based point-to-point MIMO system with residual transmit RF impairments (RTRI) using spatial multiplexing transmission. Specifically, we derive a new linear channel estimator for the proposed model, and show that RTRI create an estimation error floor in the high signal-to-noise ratio (SNR) regime. Moreover, we derive closed-form expressions for the signal-to-noise-plus-interference ratio (SINR) distributions, along with analytical expressions for the ergodic achievable rates of zero-forcing, maximum ratio combining, and minimum mean-squared error receivers, respectively. In addition, we optimize the ergodic achievable rates with respect to the training sequence length and demonstrate that finite dimensional systems with RTRI generally require more training at high SNRs than those with ideal hardware. Finally, we extend our analysis to large-scale MIMO configurations, and derive deterministic equivalents of the ergodic achievable rates. It is shown that, by deploying large receive antenna arrays, the extra training requirements due to RTRI can be eliminated. In fact, with a sufficiently large number of receive antennas, systems with RTRI may even need less training than systems with ideal hardware.

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The Magellanic Clouds are uniquely placed to study the stellar contribution to dust emission. Individual stars can be resolved in these systems even in the mid-infrared, and they are close enough to allow detection of infrared excess caused by dust. We have searched the Spitzer Space Telescope data archive for all Infrared Spectrograph (IRS) staring-mode observations of the Small Magellanic Cloud (SMC) and found that 209 Infrared Array Camera (IRAC) point sources within the footprint of the Surveying the Agents of Galaxy Evolution in the Small Magellanic Cloud (SAGE-SMC) Spitzer Legacy programme were targeted, within a total of 311 staring-mode observations. We classify these point sources using a decision tree method of object classification, based on infrared spectral features, continuum and spectral energy distribution shape, bolometric luminosity, cluster membership and variability information. We find 58 asymptotic giant branch (AGB) stars, 51 young stellar objects, 4 post-AGB objects, 22 red supergiants, 27 stars (of which 23 are dusty OB stars), 24 planetary nebulae (PNe), 10 Wolf-Rayet stars, 3 H II regions, 3 R Coronae Borealis stars, 1 Blue Supergiant and 6 other objects, including 2 foreground AGB stars. We use these classifications to evaluate the success of photometric classification methods reported in the literature.

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In this paper, we study the achievable ergodic sum-rate of multiuser multiple-input multiple-output downlink systems in Rician fading channels. We first derive a lower bound on the average signal-to-leakage-and-noise ratio by using the Mullen’s inequality, and then use it to analyze the effect of channel mean information on the achievable ergodic sum-rate. A novel statistical-eigenmode space-division multiple-access (SESDMA) downlink transmission scheme is then proposed. For this scheme, we derive an exact analytical closed-form expression for the achievable ergodic rate and present tractable tight upper and lower bounds. Based on our analysis, we gain valuable insights into the system parameters, such as the number of transmit antennas, the signal-to-noise ratio (SNR) and Rician K-factor on the system sum-rate. Results show that the sum-rate converges to a saturation value in the high SNR regime and tends to a lower limit for the low Rician K-factor case. In addition, we compare the achievable ergodic sum-rate between SE-SDMA and zeroforcing beamforming with perfect channel state information at the base station. Our results reveal that the rate gap tends to zero in the high Rician K-factor regime. Finally, numerical results are presented to validate our analysis.

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The development of 5G enabling technologies brings new challenges to the design of power amplifiers (PAs). In particular, there is a strong demand for low-cost, nonlinear PAs which, however, introduce nonlinear distortions. On the other hand, contemporary expensive PAs show great power efficiency in their nonlinear region. Inspired by this trade-off between nonlinearity distortions and efficiency, finding an optimal operating point is highly desirable. Hence, it is first necessary to fully understand how and how much the performance of multiple-input multiple-output (MIMO) systems deteriorates with PA nonlinearities. In this paper, we first reduce the ergodic achievable rate (EAR) optimization from a power allocation to a power control problem with only one optimization variable, i.e. total input power. Then, we develop a closed-form expression for the EAR, where this variable is fixed. Since this expression is intractable for further analysis, two simple lower bounds and one upper bound are proposed. These bounds enable us to find the best input power and approach the channel capacity. Finally, our simulation results evaluate the EAR of MIMO channels in the presence of nonlinearities. An important observation is that the MIMO performance can be significantly degraded if we utilize the whole power budget.

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We investigate the cell coverage optimization problem for the massive multiple-input multiple-output (MIMO) uplink. By deploying tilt-adjustable antenna arrays at the base stations, cell coverage optimization can become a promising technique which is able to strike a compromise between covering cell-edge users and pilot contamination suppression. We formulate a detailed description of this optimization problem by maximizing the cell throughput, which is shown to be mainly determined by the user distribution within several key geometrical regions. Then, the formulated problem is applied to different example scenarios: for a network with hexagonal shaped cells and uniformly distributed users, we derive an analytical lower bound of the ergodic throughput in the objective cell, based on which, it is shown that the optimal choice for the cell coverage should ensure that the coverage of different cells does not overlap; for a more generic network with sectoral shaped cells and non-uniformly distributed users, we propose an analytical approximation of the ergodic throughput. After that, a practical coverage optimization algorithm is proposed, where the optimal solution can be easily obtained through a simple one-dimensional line searching within a confined searching region. Our numerical results show that the proposed coverage optimization method is able to greatly increase the system throughput in macrocells for the massive MIMO uplink transmission, compared with the traditional schemes where the cell coverage is fixed.

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We analyze the performance of amplify-and-forward dual-hop relaying systems in the presence of in-phase and quadrature-phase imbalance (IQI) at the relay node. In particular, an exact analytical expression for and tight lower bounds on the outage probability are derived over independent, non-identically distributed Nakagami-m fading channels. Moreover, tractable upper and lower bounds on the ergodic capacity are presented at arbitrary signal-to-noise ratios (SNRs). Some special cases of practical interest (e.g., Rayleigh and Nakagami-0.5 fading) are also studied. An asymptotic analysis is performed in the high SNR regime, where we observe that IQI results in a ceiling effect on the signal-to-interference-plus-noise ratio (SINR), which depends only on the level of I/Q impairments, i.e., the joint image rejection ratio. Finally, the optimal I/Q amplitude and phase mismatch parameters are provided for maximizing the SINR ceiling, thus improving the system performance. An interesting observation is that, under a fixed total phase mismatch constraint, it is optimal to have the same level of transmitter (TX) and receiver (RX) phase mismatch at the relay node, while the optimal values for the TX and RX amplitude mismatch should be inversely proportional to each other.

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We study multicarrier multiuser multiple-input multiple-output (MU-MIMO) systems, in which the base station employs an asymptotically large number of antennas. We analyze a fully correlated channel matrix and provide a beam domain channel model, where the channel gains are independent of sub-carriers. For this model, we first derive a closed-form upper bound on the achievable ergodic sum-rate, based on which, we develop asymptotically necessary and sufficient conditions for optimal downlink transmission that require only statistical channel state information at the transmitter. Furthermore, we propose a beam division multiple access (BDMA) transmission scheme that simultaneously serves multiple users via different beams. By selecting users within non-overlapping beams, the MU-MIMO channels can be equivalently decomposed into multiple single-user MIMO channels; this scheme significantly reduces the overhead of channel estimation, as well as, the processing complexity at transceivers. For BDMA transmission, we work out an optimal pilot design criterion to minimize the mean square error (MSE) and provide optimal pilot sequences by utilizing the Zadoff-Chu sequences. Simulations demonstrate the near-optimal performance of BDMA transmission and the advantages of the proposed pilot sequences.

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Geological, biological, morphological, and hydrochemical data are presented for the newly discovered Moytirra vent field at 45oN. This is the only high temperature hydrothermal vent known between the Azores and Iceland, in the North Atlantic and is located on a slow to ultraslow-spreading mid-ocean ridge uniquely situated on the 300 m high fault scarp of the eastern axial wall, 3.5 km from the axial volcanic ridge crest. Furthermore, the Moytirra vent field is, unusually for tectonically controlled hydrothermal vents systems, basalt hosted and perched midway up on the median valley wall and presumably heated by an off-axis magma chamber. The Moytirra vent field consists of an alignment of four sites of venting, three actively emitting "black smoke," producing a complex of chimneys and beehive diffusers. The largest chimney is 18 m tall and vigorously venting. The vent fauna described here are the only ones documented for the North Atlantic (Azores to Reykjanes Ridge) and significantly expands our knowledge of North Atlantic biodiversity. The surfaces of the vent chimneys are occupied by aggregations of gastropods (Peltospira sp.) and populations of alvinocaridid shrimp (Mirocaris sp. with Rimicaris sp. also present). Other fauna present include bythograeid crabs (Segonzacia sp.) and zoarcid fish (Pachycara sp.), but bathymodiolin mussels and actinostolid anemones were not observed in the vent field. The discovery of the Moytirra vent field therefore expands the known latitudinal distributions of several vent-endemic genera in the north Atlantic, and reveals faunal affinities with vents south of the Azores rather than north of Iceland. © 2013. American Geophysical Union. All Rights Reserved.

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Background: Excessive activation of epithelial sodium channels (ENaC) contributes to CF lung pathophysiology due to the resultant dehydration of the airway surface liquid (ASL) and impaired mucociliary clearance. Regulated proteolysis of the endogenous α and γ subunits of ENaC by apical membrane-bound Channel Activating Proteases (CAPs) is a fundamental regulatory mechanism for channel activity. In the CF lung a stark imbalance between the levels of CAPs and their natural inhibitors drives the activation of normally inactive ENaC. On this basis inhibition of CAPs-ENaC signalling represents a potential therapeutic intervention. To this end we have developed a novel cell impermeable active-site directed compound (QUB-TL1) designed to inactivate key trypsin-like CAPs highly relevant in this regard. Objectives & Methods: Utilize differentiated non-CF and CF human airway epithelial cells to assess the impact of QUB-TL1 on a range of parameters including surface CAP activities, ENaC subunit processing/channel activity, ASL height and mucociliary clearance. Results: Treatment of airway epithelial cells with QUB-TL1 results in the significant downregulation of key endogenous CAP activities found to be excessively active at the surface of CF cultures. QUB-TL1-mediated CAP inhibition subsequently causes the internalisation of a pool of processed (active) ENaCγ prominent at the apical surface of CF cultures which correlates with a decline in channel activity. This downregulation of ENaC activity results in an increase in ASL height and improved mucociliary clearance in CF cells. We further find QUB-TL1 uniquely inhibits the ENaC activating enzyme furin, which is in contrast to the alternate trypsin-like CAP inhibitors camostat mesylate and aprotinin. QUB-TL1-mediated furin inhibition correlates with a reduction in neutrophil elastase-induced ENaC activation. Moreover we find QUB-TL1 treatment protects CF cultures from Pseudomonas aeruginosa exotoxin A-induced cytotoxicity. Pseudomonas aeruginosa exotoxin A is a major toxic product activated by furin and positively associated with mortality. Conclusion: The novel inhibitor (QUB-TL1) dampens CAPs-ENaC signalling which improves hydration status mucociliary clearance in CF airway epithelial cell cultures. Moreover this compound provides additional benefit by preventing Pseudomonas aeruginosa exotoxin A-induced cytotoxicity.

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Background: Oncogenic mutations in BRAF occur in 8% of patients with advanced colorectal cancer (CRC) and have been shown to correlate with poor prognosis. In contrast to BRAF mutant (MT) melanoma, where the BRAF inhibitor Vemurafenib (PLX4032) has shown significant increases in response rates and overall survival, only minor responses to Vemurafenib treatment have been reported in BRAFMT CRC. Clear understanding of the vulnerabilities of BRAFMT CRC is important, and identification of druggable targets uniquely required by BRAFMT CRC tumours has the potential to fill a gap in the therapeutic armamentarium of advanced CRC. The aim of this study was to identify novel resistance mechanisms to MEK inhibition in BRAFMT CRC. Methods: Paired BRAFMT/WT RKO and VACO432 CRC cells and non-isogenic BRAFMT LIM2405, WiDR, HT-29 and COLO205 CRC cells were used. Changes in protein expression/activity were assessed by Western Blotting. Interactions between MEK1/2 and JAK1/2 or c-MET inhibition were assessed using the MTT cell viability assays and Flow Cytometry. Apoptosis was measured using Western Blotting for PARP, cleaved caspase 3, 8 and 9, and caspase 3/7 and 8 activity assays. Results: Treatment with MEK1/2 inhibitors AZD6244, trametinib, UO126 and PD98059 resulted in acute increases in STAT3 activity in the BRAFMT RKO and VACO432 cells but not in their BRAFWT clones and this was associated with increases in JAK2 activity. Inhibition of JAK/STAT3 activation using gene specific siRNA or small molecule inhibitors TG101348 or AZD1480, abrogated this survival response and resulted in synergy and significant increases in cell death when combined with MEK1/2 inhibitors AZD6244 or trametinib in BRAFMT CRC cells. The RTK c-MET is activated upstream of STAT3 following MEK1/2 inhibition. Inhibition of c-MET and MEK1/2, using pharmacological inhibitors (crizotinib and AZD6244), results in synergy and increased cell death in BRAFMT CRC cells. Conclusions: We have identified JAK/STAT3 activation as an important escape mechanism for BRAFMT CRC following MEK1/2 inhibition in vitro. Combinations of JAK/MEKi or MET/MEKi can be a potential novel treatment strategy for poor prognostic BRAFMT advanced CRC patients.

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The transposition of the 2002/14/EC Directive, establishing a general framework for information and consultation (I&C), has proven contentious in largely voluntarist systems of employment regulation. Receiving particular criticism is the employee ‘opt-in’ mechanism as a means to access I&C rights. For non-union employees in particular, the ability and potential to negotiate rights for I&C is widely seen to be problematic. This article uniquely examines the opt-in mechanism in the context of non-unionism, considering how non-union employers respond to non-union employees invoking their legislative rights to I&C. Drawing upon a case study conducted over four years in a large non-union multinational, the evidence shows how the opt-in and negotiation process function to the advantage of the employer rather than the intended regulatory impact to advance employee rights