32 research outputs found

    Convergence analysis of blind equalization algorithms using constellation-matching

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    Two modified blind equalization algorithms are analyzed for performance. These algorithms add a constellation-matched error term to the cost functions of the generalized Sato and multimodulus algorithms. The dynamic convergence behavior and steady-state performance of these algorithms, and of a related version of the constant modulus algorithm, are characterized. The analysis establishes the improved performance of the proposed algorithms

    Robust Techniques for Signal Processing: A Survey

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    Coordinated Science Laboratory was formerly known as Control Systems LaboratoryU.S. Army Research Office / DAAG29-81-K-0062U.S. Air Force Office of Scientific Research / AFOSR 82-0022Joint Services Electronics Program / N00014-84-C-0149National Science Foundation / ECS-82-12080U.S. Office of Naval Research / N00014-80-K-0945 and N00014-81-K-001

    A Wideband, Synthetic Aperture Beamformer for Through-The-Wall Imaging

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    A coarray-based aperture synthesis scheme using subarrays and post-data acquisition beamforming is presented for through-the-wall wideband microwave imaging applications. Various effects of the presence of the wall, such as refraction, change in speed, and attenuation, are incorporated into the beamformer design. Simulation results verifying the proposed synthetic aperture technique for a TWI system are presented. The effects of incorrect estimates of the parameters of the wall, such as thickness and dielectric constant, on performance are investigated

    Design and Implementation of Near-Field, Wideband Synthetic Aperture Beamformers

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    A coarray-based near-field, wideband synthetic aperture beamformer using stepped-frequency signal synthesis and post-data acquisition processing is presented. While coarray techniques offer significant reduction in the number of array elements for a given angular resolution, the hybrid subarray-stepped frequency realization of wideband systems simplifies implementations and offers flexibility in beamforming. Proof of concept is provided using real data collected in an anechoic chamber for several pulse shapes and array weightings

    A New Approach for Near-Field Wideband Synthetic Aperture Beamforming

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    A coarray-based synthetic aperture beamformer using stepped-frequency signal synthesis and post-data acquisition processing is presented for wideband imaging of near-field scenes. The proposed beamformer formulation and implementation finds key applications in through-the-wall microwave imaging and landmine detection problems. While coarray techniques offer significant reduction in array elements for a given angular resolution, stepped-frequency realization of wideband systems simplifies implementation and offers flexibility in beamforming. Proof of concept is provided using real data collected in an anechoic chamber

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Signal detection in non-Gaussian noise

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