3,887 research outputs found
Inversion of Parahermitian matrices
Parahermitian matrices arise in broadband multiple-input multiple-output (MIMO) systems or array processing, and require inversion in some instances. In this paper, we apply a polynomial eigenvalue decomposition obtained by the sequential best rotation algorithm to decompose a parahermitian matrix into a product of two paraunitary, i.e.lossless and easily invertible matrices, and a diagonal polynomial matrix. The inversion of the overall parahermitian matrix therefore reduces to the inversion of auto-correlation sequences in this diagonal matrix. We investigate a number of different approaches to obtain this inversion, and and assessment of the numerical stability and complexity of the inversion process
Training based channel estimation algorithms for dual hop MIMO OFDM relay systems
In this paper we consider minimum mean square error (MMSE) training based channel estimation for two-hop multiple-input multiple-output (MIMO) orthogonal frequency division multiplexing (OFDM) relaying systems. The channel estimation process is divided into two main phases. The relay-destination channel is estimated in the first phase and can be obtained using well known point-to-point MIMO OFDM estimation methods. In the second phase, the source-relay channel is estimated at the destination with the use of a known training sequence that is transmitted from the source and forwarded to the destination by a non-regenerative relay. To obtain an estimate of the source-relay channel, the source training sequence, relay precoder, and destination processor, require to be optimised. To solve this problem we derive an iterative algorithm that involves sequentially solving a number of convex optimisation problems to update the source, relay, and destination design variables. Since the iterative algorithm may be too computationally expensive for practical implementation we then derive simplified solutions that have reduced computational complexity. Simulation results demonstrate the effectiveness of the proposed algorithms
So near and yet so far: Harmonic radar reveals reduced homing ability of nosema infected honeybees
Pathogens may gain a fitness advantage through manipulation of the behaviour of their hosts. Likewise, host behavioural changes can be a defence mechanism, counteracting the impact of pathogens on host fitness. We apply harmonic radar technology to characterize the impact of an emerging pathogen - Nosema ceranae (Microsporidia) - on honeybee (Apis mellifera) flight and orientation performance in the field. Honeybees are the most important commercial pollinators. Emerging diseases have been proposed to play a prominent role in colony decline, partly through sub-lethal behavioural manipulation of their hosts. We found that homing success was significantly reduced in diseased (65.8%) versus healthy foragers (92.5%). Although lost bees had significantly reduced continuous flight times and prolonged resting times, other flight characteristics and navigational abilities showed no significant difference between infected and non-infected bees. Our results suggest that infected bees express normal flight characteristics but are constrained in their homing ability, potentially compromising the colony by reducing its resource inputs, but also counteracting the intra-colony spread of infection. We provide the first high-resolution analysis of sub-lethal effects of an emerging disease on insect flight behaviour. The potential causes and the implications for both host and parasite are discussed
So near and yet so far: Harmonic radar reveals reduced homing ability of nosema infected honeybees
Pathogens may gain a fitness advantage through manipulation of the behaviour of their hosts. Likewise, host behavioural changes can be a defence mechanism, counteracting the impact of pathogens on host fitness. We apply harmonic radar technology to characterize the impact of an emerging pathogen - Nosema ceranae (Microsporidia) - on honeybee (Apis mellifera) flight and orientation performance in the field. Honeybees are the most important commercial pollinators. Emerging diseases have been proposed to play a prominent role in colony decline, partly through sub-lethal behavioural manipulation of their hosts. We found that homing success was significantly reduced in diseased (65.8%) versus healthy foragers (92.5%). Although lost bees had significantly reduced continuous flight times and prolonged resting times, other flight characteristics and navigational abilities showed no significant difference between infected and non-infected bees. Our results suggest that infected bees express normal flight characteristics but are constrained in their homing ability, potentially compromising the colony by reducing its resource inputs, but also counteracting the intra-colony spread of infection. We provide the first high-resolution analysis of sub-lethal effects of an emerging disease on insect flight behaviour. The potential causes and the implications for both host and parasite are discussed
Boundary Zonal Flow in Rotating Turbulent Rayleigh-Bénard Convection
For rapidly rotating turbulent Rayleigh–Bénard convection in a slender cylindrical cell, experiments and direct numerical simulations reveal a boundary zonal flow (BZF) that replaces the classical large-scale circulation. The BZF is located near the vertical side wall and enables enhanced heat transport there. Although the azimuthal velocity of the BZF is cyclonic (in the rotating frame), the temperature is an anticyclonic traveling wave of mode one, whose signature is a bimodal temperature distribution near the radial boundary. The BZF width is found to scale like Ra1/4Ek2/3 where the Ekman number Ek decreases with increasing rotation rate
Ischemia and reperfusion injury in kidney transplantation : relevant mechanisms in injury and repair
Ischemia and reperfusion injury (IRI) is a complex pathophysiological phenomenon, inevitable in kidney transplantation and one of the most important mechanisms for non- or delayed function immediately after transplantation. Long term, it is associated with acute rejection and chronic graft dysfunction due to interstitial fibrosis and tubular atrophy. Recently, more insight has been gained in the underlying molecular pathways and signalling cascades involved, which opens the door to new therapeutic opportunities aiming to reduce IRI and improve graft survival. This review systemically discusses the specific molecular pathways involved in the pathophysiology of IRI and highlights new therapeutic strategies targeting these pathways
Role of Stromal Cells in Protecting Young and Aged B-Lineage Precursors from Dexamethasone-Induced Apoptosis
Maximum diameter measurements of aortic aneurysms on axial CT images after endovascular aneurysm repair: sufficient for follow-up?
PURPOSE: To assess the accuracy of maximum diameter measurements of aortic aneurysms after endovascular aneurysm repair (EVAR) on axial computed tomographic (CT) images in comparison to maximum diameter measurements perpendicular to the intravascular centerline for follow-up by using three-dimensional (3D) volume measurements as the reference standard. MATERIALS AND METHODS: Forty-nine consecutive patients (73 ± 7.5 years, range 51-88 years), who underwent EVAR of an infrarenal aortic aneurysm were retrospectively included. Two blinded readers twice independently measured the maximum aneurysm diameter on axial CT images performed at discharge, and at 1 and 2 years after intervention. The maximum diameter perpendicular to the centerline was automatically measured. Volumes of the aortic aneurysms were calculated by dedicated semiautomated 3D segmentation software (3surgery, 3mensio, the Netherlands). Changes in diameter of 0.5 cm and in volume of 10% were considered clinically significant. Intra- and interobserver agreements were calculated by intraclass correlations (ICC) in a random effects analysis of variance. The two unidimensional measurement methods were correlated to the reference standard. RESULTS: Intra- and interobserver agreements for maximum aneurysm diameter measurements were excellent (ICC = 0.98 and ICC = 0.96, respectively). There was an excellent correlation between maximum aneurysm diameters measured on axial CT images and 3D volume measurements (r = 0.93, P < 0.001) as well as between maximum diameter measurements perpendicular to the centerline and 3D volume measurements (r = 0.93, P < 0.001). CONCLUSION: Measurements of maximum aneurysm diameters on axial CT images are an accurate, reliable, and robust method for follow-up after EVAR and can be used in daily routine
Adenovirus triggers macropinocytosis and endosomal leakage together with its clathrin-mediated uptake
Adenovirus type 2 (Ad2) binds the coxsackie B virus Ad receptor and is endocytosed upon activation of the αv integrin coreceptors. Here, we demonstrate that expression of dominant negative clathrin hub, eps15, or K44A-dynamin (dyn) inhibited Ad2 uptake into epithelial cells, indicating clathrin-dependent viral endocytosis. Surprisingly, Ad strongly stimulated the endocytic uptake of fluid phase tracers, coincident with virus internalization but without affecting receptor-mediated transferrin uptake. A large amount of the stimulated endocytic activity was macropinocytosis. Macropinocytosis depended on αv integrins, PKC, F-actin, and the amiloride-sensitive Na+/H+ exchanger, which are all required for Ad escape from endosomes and infection. Macropinocytosis stimulation was not a consequence of viral escape, since it occurred in K44A-dyn–expressing cells. Surprisingly, 30–50% of the endosomal contents were released into the cytosol of control and also K44A-dyn–expressing cells, and the number of fluid phase–positive endosomes dropped below the levels of noninfected cells, indicating macropinosomal lysis. The release of macropinosomal contents was Ad dose dependent, but the presence of Ad particles on macropinosomal membranes was not sufficient for contents release. We conclude that Ad signaling from the cell surface controls the induction of macropinosome formation and leakage, and this correlates with viral exit to the cytosol and infection
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