55 research outputs found

    A note on Hardy-Littlewood maximal operators

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    IL-17RA Is Required for CCL2 Expression, Macrophage Recruitment, and Emphysema in Response to Cigarette Smoke

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    Chronic Obstructive Pulmonary Disease (COPD) is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and in vivo Th17, but not Th1, cell differentiation via the aryl hydrocarbon receptor. Smoke exposed IL-17RA−/− mice failed to induce CCL2 and MMP12 compared to WT mice. Remarkably, in contrast to WT mice, IL-17RA−/− mice failed to develop emphysema after 6 months of cigarette smoke exposure. Taken together, these data demonstrate that cigarette smoke is a potent Th17 adjuvant and that IL-17RA signaling is required for chemokine expression necessary for MMP12 induction and tissue emphysema

    Inflammatory Cells as a Source of Airspace Extracellular Superoxide Dismutase after Pulmonary Injury

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    Extracellular superoxide dismutase (EC-SOD) is an antioxidant abundant in the lung. Previous studies demonstrated depletion of lung parenchymal EC-SOD in mouse models of interstitial lung disease coinciding with an accumulation of EC-SOD in airspaces. EC-SOD sticks to the matrix by a proteolytically sensitive heparin-binding domain; therefore, we hypothesized that interstitial inflammation and matrix remodeling contribute to proteolytic redistribution of EC-SOD from lung parenchyma into the airspaces. To determine if inflammation limited to airspaces leads to EC-SOD redistribution, we examined a bacterial pneumonia model. This model led to increases in airspace polymorphonuclear leukocytes staining strongly for EC-SOD. EC-SOD accumulated in airspaces at 24 h without depletion of EC-SOD from lung parenchyma. This led us to hypothesize that airspace EC-SOD was released from inflammatory cells and was not a redistribution of matrix EC-SOD. To test this hypothesis, transgenic mice with lung-specific expression of human EC-SOD were treated with asbestos or bleomycin to initiate an interstitial lung injury. In these studies, EC-SOD accumulating in airspaces was entirely the mouse isoform, demonstrating an extrapulmonary source (inflammatory cells) for this EC-SOD. We also demonstrate that EC-SOD knockout mice possess greater lung inflammation in response to bleomycin and bacteria when compared with wild types. We conclude that the source of accumulating EC-SOD in airspaces in interstitial lung disease is inflammatory cells and not the lung and that interstitial processes such as those found in pulmonary fibrosis are required to remove EC-SOD from lung matrix

    Two-dimensional superconductivity realized in an MBE-grown Bi2Te3/FeTe heterostructure

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    We report a superconductivity realized at the interface of a Bi2Te3/FeTe heterostructure fabricated via van der Waals epitaxy using the molecular beam epitaxy technique, which appears even when the thickness of Bi2Te3 is as thin as one quintuple layer. The two-dimensional nature of the observed superconductivity with the highest transition temperature around 12 K was verified by the existence of a Berezinsky-Kosterlitz-Thouless transition and the diverging ratio of in-plane to out-plane upper critical field on approaching the superconducting transition temperature. The underlying mechanism of this interfacial superconductivity will be discussed. The heterostructure studied in this work provides an ideal platform with unconventional superconductivity for hosting Majorana fermions and studying their exotic physics

    Rigid blocks matching method based on contour curves and feature regions

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    This study proposes a blocks matching method based on contour curves and feature regions that improve the matching precision and speed with which rigid blocks with a specified thickness in point clouds are matched. The method comprises two steps: coarse matching and fine matching. In the coarse matching step, the rigid blocks are first segmented into a series of surfaces and the fracture surfaces are distinguished. Then, the contour curves of the fracture surfaces are extracted using an improved boundary growth method and the rigid blocks are coarsely matched with them. In the fine matching step, feature regions are first extracted from the fracture surfaces. Then, the centroid of each feature region is calculated and the fine matching of rigid blocks with the centroid sets is completed using an improved iterative closest point (ICP) algorithm. The improved ICP algorithm integrates the rotation angle constraint and dynamic iteration coefficient into a probability ICP algorithm, which significantly improves matching precision and speed. Experiments conducted using public blocks and Terracotta Warriors blocks indicate that the proposed method carries out rigid blocks matching more accurately and rapidly than various conventional methods
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