Adversarial Patch Camouflage against Aerial Detection

Detection of military assets on the ground can be performed by applying deep learning-based object detectors on drone surveillance footage. The traditional way of hiding military assets from sight is camouflage, for example by using camouflage nets. However, large assets like planes or vessels are difficult to conceal by means of traditional camouflage nets. An alternative type of camouflage is the direct misleading of automatic object detectors. Recently, it has been observed that small adversarial changes applied to images of the object can produce erroneous output by deep learning-based detectors. In particular, adversarial attacks have been successfully demonstrated to prohibit person detections in images, requiring a patch with a specific pattern held up in front of the person, thereby essentially camouflaging the person for the detector. Research into this type of patch attacks is still limited and several questions related to the optimal patch configuration remain open. This work makes two contributions. First, we apply patch-based adversarial attacks for the use case of unmanned aerial surveillance, where the patch is laid on top of large military assets, camouflaging them from automatic detectors running over the imagery. The patch can prevent automatic detection of the whole object while only covering a small part of it. Second, we perform several experiments with different patch configurations, varying their size, position, number and saliency. Our results show that adversarial patch attacks form a realistic alternative to traditional camouflage activities, and should therefore be considered in the automated analysis of aerial surveillance imagery.Comment: 9 page

Aggravation of Anti-Myeloperoxidase Antibody-Induced Glomerulonephritis by Bacterial Lipopolysaccharide : Role of Tumor Necrosis Factor-α

Wegener’s granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome, and idiopathic pauci-immune necrotizing crescentic glomerulonephritis are associated with myeloperoxidase (MPO)-specific anti-neutrophil cytoplasmic autoantibodies (ANCAs). Clinical and experimental evidence indicates that ANCA and proinflammatory stimuli of infectious origin act synergistically to cause vasculitis. We tested this hypothesis in a recently developed mouse model of anti-MPO IgG-induced glomerulonephritis by using bacterial lipopolysaccharide (LPS) as the proinflammatory stimulus. Systemic administration of LPS dose dependently increased renal injury induced by anti-MPO IgG as demonstrated by increased glomerular crescent formation and glomerular necrosis. In the early phase, LPS enhanced anti-MPO IgG-induced glomerular neutrophil accumulation. Furthermore, a transient induction of circulating tumor necrosis factor (TNF)-α levels, followed by a marked increase in circulating MPO levels, was observed on administration of LPS. In vitro, anti-MPO IgG induced a respiratory burst in murine neutrophils only after priming with TNF-α. Finally, anti-TNF-α treatment attenuated, but did not prevent, the LPS-mediated aggravation of anti-MPO IgG-induced glomerulonephritis. In conclusion, our study demonstrates that ANCA and proinflammatory stimuli act synergistically to induce vasculitic disease and suggests potential benefits of inhibiting TNF-α bioactivity in treating human ANCA-associated necrotizing crescentic glomerulonephritis

Arginase-1 deficiency regulates arginine concentrations and NOS2-mediated NO production during endotoxemia

Arginase-1 is an important component of the intricate mechanism regulating arginine availability during immune responses and nitric oxide synthase (NOS) activity. In this study Arg1(fl/fl)/Tie2-Cre(tg/-) mice were developed to investigate the effect of arginase-1 related arginine depletion on NOS2- and NOS3-dependent NO production and jejunal microcirculation under resting and endotoxemic conditions, in mice lacking arginase-1 in endothelial and hematopoietic cells. Arginase-1-deficient mice as compared with control mice exhibited higher plasma arginine concentration concomitant with enhanced NO production in endothelial cells and jejunal tissue during endotoxemia. In parallel, impaired jejunal microcirculation was observed in endotoxemic conditions. Cultured bone-marrow-derived macrophages of arginase-1 deficient animals also presented a higher inflammatory response to endotoxin than control littermates. Since NOS2 competes with arginase for their common substrate arginine during endotoxemia, Nos2 deficient mice were also studied under endotoxemic conditions. As Nos2(-/-) macrophages showed an impaired inflammatory response to endotoxin compared to wild-type macrophages, NOS2 is potentially involved. A strongly reduced NO production in Arg1(fl/fl)/Tie2-Cre(tg/-) mice following infusion of the NOS2 inhibitor 1400W further implicated NOS2 in the enhanced capacity to produce NO production Arg1(fl/fl)/Tie2-Cre(tg/-) mice. Reduced arginase-1 activity in Arg1(fl/fl)/Tie2-Cre(tg/-) mice resulted in increased inflammatory response and NO production by NOS2, accompanied by a depressed microcirculatory flow during endotoxemia. Thus, arginase-1 deficiency facilitates a NOS2-mediated pro-inflammatory activity at the expense of NOS3-mediated endothelial relaxatio

Impaired nitrite, TNF, IL-10 and IL-12p40 production in cultured <i>Nos2^−/−</i> bone marrow-derived macrophages after LPS stimulation.

<p>(A) LPS-treated bone marrow-derived macrophages from <i>Nos2^−/−</i> mice (n = 3) produced less nitrite (A; P<0.001), TNF (B; P<0.01), and IL-12p40 (D; P<0.01) in 24 hrs than macrophages from control mice (n = 3). IL-10 production after LPS treatment did not differ between control and <i>Nos2^−/−</i> macrophages (C).</p

Relative mRNA expression in control and <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice under physiological and endotoxemic conditions.

<p>(A) Relative <i>Arg1</i> mRNA expression was significantly higher in the control + LPS group than in basal and <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> + LPS groups. As expected, <i>Arg1</i> expression was low in <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice. (B) Interestingly, the relative <i>Arg2</i> mRNA expression was significantly higher in the <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice after LPS infusion compared to control mice during endotoxemic conditions. (C) LPS infusion resulted in increased <i>Nos2</i> expression in both mouse strains compared to basal conditions. (D) <i>Nos3</i> mRNA expression was significantly higher in the <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice compared to control animals under basal and LPS-infused conditions (p<0.05). The relative expression of the two household genes <i>Actb</i> and <i>Ppia</i> were used to calculate the geometric mean, which served as a normalization factor.</p

Plasma arginine, citrulline and ornithine amino-acid concentrations in control and <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice under basal and endotoxemic conditions.

<p>Plasma concentrations are displayed in µmol/L. Values are represented as mean ± SEM. Significance: *p<0.05 vs. control during basal conditions; $p<0.001 vs. <i>Arg1^fl/fl/Tie2-Cre^tg/−</i>during basal conditions; ^#p<0.001 vs. <i>Arg1^fl/fl/Tie2-Cre^tg/−+ LPS</i>.</p

Number of perfused vessels per villus under basal conditions and after LPS treatment in control, <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> and <i>Nos2^−/−</i> mice.

<p>Number of perfused vessels was determined with SDF-imaging. Fewer vessels per villus were perfused in <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice than in control and <i>Nos2^−/−</i> mice, both under basal conditions and after LPS treatment. LPS infusion decreased the number of perfused vessels per villus in all three mouse strains (all n = 7).</p

LPS treatment increases density of MPO-positive cells in <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice.

<p>(A) LPS infusion increased the influx of MPO-positive cells into jejunal tissue of control and <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice, but more so in <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice (P<0.05). Magnification 200x. (B) Jejunal villi of H&E- (upper panel) and MPO-stained (lower panel) villi of LPS-treated control (left) and <i>Arg1^fl/fl/Tie2-Cre^tg/−</i> mice (right). Arrows indicate the MPO positive cells. Magnification 200x.</p