Abstract-Synthetic Aperture Radar (SAR) can obtain a twodimensional image of the observed scene. However, the resolution of conventional SAR imaging algorithm based on Matched Filter (MF) theory is limited by the transmitted signal bandwidth and the antenna length. Compressed sensing (CS) is a new approach of sparse signals recovered beyond the Nyquist sampling constraints. In this paper, a high resolution imaging method is presented for SAR sparse targets reconstruction based on CS theory. It shows that the image of sparse targets can be reconstructed by solving a convex optimization problem based on L1 norm minimization with only a small number of SAR echo samples. This indicates the sample size of SAR echo can be considerably reduced by CS method. Super-resolution property and point-localization ability are demonstrated using simulated data. Numerical results show the presented CS method outperforms the conventional SAR algorithm based on MF even though small sample size of SAR echo is used in this method.

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Abstract-Microwave array 3-D imaging is an emerging technique capable of producing a 3-D map of scattered electric fields. Its all-weather and large scene imaging features make it an attractive powerful tool for target detection and feature extraction. Typically, a microwave array 3-D imaging system based on the classical sampling theory requires a large dense 2-D antenna array, which may suffer from a very high cost. To reduce the number of the antenna array elements, this paper surveys the use of compressed sensing recovery and sparse measurement strategies for microwave array 3-D imaging. Combining with the typical spatial sparsity of the underlying scene, we pose the sparse array microwave 3-D imaging as finding sparse solutions to under-determined linear equations. Further, to reduce the computational of the compressed sensing recovery with the largescale echoes data, we divide the underlying 3-D scene into a series of equal-range 2-D slices, and deal with these slices separately using the orthogonal matching pursuit (OMP) algorithm. Lastly, the performance of the presented compressed sensing approach is verified by an X-band microwave array 3-D imaging system. The experimental results demonstrate that the compressed sensing approach can produce a better resolution 3-D image of the observed scatterers compared with the conventional method, especially in the case of very sparse activate antenna array.

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Background: Both endoplasmic reticulum (ER) stress and macrophage diversity contribute to inflammatory processes in lung injury. However, the interaction between ER stress and macrophage M1/M2 imbalance in lung inflammation remains unclear. The present study, thus, aimed to evaluate the role of ER stress-mediated macrophage phenotype changes in lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods: Lung inflammation and injury were examined in a murine model of LPS-induced ALI with or without ER stress inhibitors. Alveolar macrophage (AM) polarization was determined by flow cytometry.Bone marrow-derived macrophages (BMDMs) were treated with either an ER stress inducer, inhibitor, or an IRE-1 endonuclease inhibitor before being polarized to an M1 and M2 phenotype. The macrophage polarization status was examined via RT-PCR and flow cytometry.Results: Our results indicated that ER stress and IRE-1/XBP-1 signaling are activated in LPS-induced ALI. Furthermore, we observed that AM polarizes to an inflammatory phenotype upon exposure to LPS in the induction phase and an anti-inflammatory phenotype in the resolution phase of lung inflammation.Inhibition of ER stress attenuated the pathophysiological features of LPS-induced lung inflammation/injury, as evidenced by a decrease in bronchoalveolar lavage (BAL) protein levels, the number of inflammatory cells, and the expression level of inflammatory mediators. In addition, the ER stress inducer promoted M1 polarization and the switch from M2 to M1 in BMDMs, whereas inhibition of ER stress and XBP-1 splicing suppressed M1 but did not promote M2, both in vivo and in vitro.Conclusions: Our results demonstrated that inhibition of the ER stress-associated IRE-1/XBP-1 signaling pathway suppresses M1 polarization and ameliorates LPS-induced lung injury. This indicates that the interaction between ER stress and macrophage polarization might be a novel therapeutic target for endotoxin-induced lung inflammatory disorders.