DADFNet: Dual Attention and Dual Frequency-Guided Dehazing Network for Video-Empowered Intelligent Transportation

Visual surveillance technology is an indispensable functional component of advanced traffic management systems. It has been applied to perform traffic supervision tasks, such as object detection, tracking and recognition. However, adverse weather conditions, e.g., fog, haze and mist, pose severe challenges for video-based transportation surveillance. To eliminate the influences of adverse weather conditions, we propose a dual attention and dual frequency-guided dehazing network (termed DADFNet) for real-time visibility enhancement. It consists of a dual attention module (DAM) and a high-low frequency-guided sub-net (HLFN) to jointly consider the attention and frequency mapping to guide haze-free scene reconstruction. Extensive experiments on both synthetic and real-world images demonstrate the superiority of DADFNet over state-of-the-art methods in terms of visibility enhancement and improvement in detection accuracy. Furthermore, DADFNet only takes $6.3$ ms to process a 1,920 * 1,080 image on the 2080 Ti GPU, making it highly efficient for deployment in intelligent transportation systems.Comment: This paper is accepted by AAAI 2022 Workshop: AI for Transportatio

Gender differences in plaque characteristics of nonculprit lesions in patients with coronary artery disease

Abstract Background Although numerous reports suggest sex-related differences in atherosclerosis, limited data describing gender-associated differences in plaque morphology and composition are currently available. The aim of the present study was to compare coronary nonculprit plaque characteristics in women and men with coronary artery disease (CAD) by optical coherence tomography (OCT). Methods This was a retrospective study. A total of 187 nonculprit plaques were identified in 103 patients with CAD who underwent OCT imaging of all 3 coronary arteries. These patients included 77 (74.8%) men and 26 (25.2%) women. Results Female patients were significantly older than males (mean age, 70.8 ± 7.3 vs 60.8 ± 9.8 years; P < 0.001) and less likely to be current smokers (P = 0.007). OCT analysis included the presence of lipid-rich plaque, maximum lipid arc, lipid-core length, lipid index (LI), fibrous cap thickness, and the incidence of thin-cap fibroatheroma (TCFA). Nonculprit plaques in men exhibited greater lipid-core length and LI compared with those of women (9.4 ± 4.5 vs. 7.3 ± 4.3 mm, P = 0.024; 1615.1 ± 893.8 vs. 1237.8 ± 859.8, P = 0.035, respectively). In the univariate linear regression model, sex and current smoker were all associated with a larger LI, whereas only use of statin was independent risk factor for a larger LI in multivariate analysis. Conclusions Coronary nonculprit plaques in male patients with CAD contain larger lipid cores than those of female patients

Blockchain-based Federated Learning for Industrial Metaverses: Incentive Scheme with Optimal AoI

The emerging industrial metaverses realize the mapping and expanding operations of physical industry into virtual space for significantly upgrading intelligent manufacturing. The industrial metaverses obtain data from various production and operation lines by Industrial Internet of Things (IIoT), and thus conduct effective data analysis and decision-making, thereby enhancing the production efficiency of the physical space, reducing operating costs, and maximizing commercial value. However, there still exist bottlenecks when integrating metaverses into IIoT, such as the privacy leakage of sensitive data with commercial secrets, IIoT sensing data freshness, and incentives for sharing these data. In this paper, we design a user-defined privacy-preserving framework with decentralized federated learning for the industrial metaverses. To further improve privacy protection of industrial metaverse, a cross-chain empowered federated learning framework is further utilized to perform decentralized, secure, and privacy-preserving data training on both physical and virtual spaces through a hierarchical blockchain architecture with a main chain and multiple subchains. Moreover, we introduce the age of information as the data freshness metric and thus design an age-based contract model to motivate data sensing among IIoT nodes. Numerical results indicate the efficiency of the proposed framework and incentive mechanism in the industrial metaverse

The immunosuppressant Protosappanin A diminished recipient T cell migration into allograft via inhibition of IP-10 in rat heart transplant.

The immunosuppressant Protosappanin A (PrA), isolated from the medicinal herb, promotes cardiac allograft survival, diminishes inflammatory cell infiltration, and inhibits interferon γ-induced protein 10 kDa (IP-10) mRNA expression in rats cardiac grafts. Binding of the chemokine IP-10 to its cognate receptor, CXCR3, plays crucial roles in allograft immunity, especially by mediating the recruitment of effector T cells to allografted tissues. In this study, we attempted to determine whether PrA-mediated inhibition of IP-10 contributes to the effect of reduced T cell infiltration into cardiac allograft within a rat model. Administration of PrA (25 mg/kg daily) via oral gavage following heart transplantation significantly reduced the increase of IP-10 mRNA level in allograft and prevented IP-10 secretion by peripheral blood mononuclear cells (PBMC) isolated from recipient rats seven days posttransplantation. Furthermore, in vitro experiments demonstrated that PrA addition to control PBMC prevented IP-10 secretion. Chemotactic migration assays were utilized to evaluate recipient T cell migration towards PBMC supernatant. PrA administration impaired PBMC supernatant-induced T cell migration. Additional in vitro experiments revealed that PrA slightly reduced naïve T cell migration towards chemokines. The presence of IP-10 in PBMC supernatant prevented PrA from reducing T cell migration in PrA-treated recipients. Neither CXCR3 chemokine ligand Mig nor non-CXCR3 chemokine ligand SDF-1 had any effect on T cell migration in PrA-treated recipients. The addition of anti-CXCR3 antibody restored PrA-mediated inhibition of T cell migration. Immunofluorescence microscopy showed that IP-10 was expressed mainly in CD68 positive infiltrating monocytes. Furthermore, PrA consistently reduced CXCR3+T cell infiltration into cardiac allografts. The reduced intensity of CXCR3 staining in PrA-treated allografts contributed to the previously depressed naïve T cell migrating activity induced by PrA. Collectively, these data indicate that PrA inhibition of IP-10 activity reduced recipient T cell migration and infiltration of cardiac allografts, thus partially explaining the immunosuppressive effect of PrA

IRGM/Irgm1 deficiency inhibits neutrophil-platelet interactions and thrombosis in experimental atherosclerosis and arterial injury

Background: Neutrophil extracellular traps (NETs) closely link inflammation and thrombosis. The immune-related GTPase family M protein (IRGM) and its ortholog of mouse IRGM1 are positively correlated with plaque rupture during atherosclerosis process. However, whether and how IRGM/IRGM1 affects NETs formation and atherosclerotic thrombosis remains unknown, which will further promote the development of antithrombotic treatment tools. Methods: The thrombi images, platelet activation makers and NETs makers were detected in the serum of STEMI patients and controls. To futher investigate IRGM/IRGM1 affects NETs formation and atherothrombosis in vivo, ApoE-/-Irgm1+/- and ApoE-/- mice received diets rich in fat and 2.5% FeCl3 was then used to induce experimental arterial thrombosis in an atherosclerosis background. In vitro, PMA and thrombin were used to stimulate neutrophils and platelets, respectively, and the expression of IRGM/IRGM1 were modified. To reveal the molecular mechanisms, MAPK-cPLA2 signals inhibitors were used. Results: Serum IRGM was positively correlated with PF4 and neutrophil elastase. Subsequently, Irgm1 deficient mice have a longer occlusion time and lower growth rate. In vitro, as expected, IRGM/Irgm1 deficiency inhibits platelet activation and platelet-neutrophil interaction. More importantly, IRGM promoted NETs production through activating MAPK-cPLA2 signals in PMA stimulated neuropils, whereas inhibiting the production of NETs eliminated the difference in platelet activation and thrombosis caused by IRGM/Irgm1 modification in vivo and vitro. Similarly, inhibition of platelet activation also eliminated the influence of IRGM/Irgm1 modification on NETs production. Conclusions: Overall, our data indicate that IRGM/Irgm1 deficiency in neuropils inhibits the intense interaction between neutrophils and platelets, and ultimately inhibits thrombosis

PrA reduced T cell migration to PBMC supernatant through inhibition of IP-10-CXCR3 receptor interaction.

<p>IP-10 (50 ng/ml), Mig (100 ng/ml), or SDF-1 (100 ng/ml) was added to the PBMC supernatant. T cells were incubated with the isotype control Ab (20 µg/ml) or anti-CXCR3 Ab (20 µg/ml) prior to chemotactic migration assays (n = 3 in each group). (A) IP-10 addition to the supernatant of PrA-exposed PBMCs improved the migration of PrA-treated recipients T cells. Furthermore, addition of anti-CXCR3 Ab restored PrA inhibition of IP-10-induced T cell migration, but isotype Ab did not have the same effect. (B) The addition of Mig and SDF-1 did not significantly increase the migration of PrA-treated recipients T cells. However the addition of Mig, but not SDF-1 addition increased the migration of non PrA-treated recipients T cells. *indicates <i>p</i><0.05, and bars indicate comparators.</p

PrA inhibited IP-10 expression in infiltrating monocytes of cardiac allografts.

<p>Immunofluorescence staining of heart allograft sections stained with Abs to CD68 (FITC, green) and IP-10 (TMRITC, red). Nuclei were counterstained with DAPI (blue). The IP-10 expression in CD68 positive infiltrating monocytes was reduced after PrA treatment. The results are representative of three independent experiments (n = 3).</p

The migrating capacity of naïve T cells was slightly affected by PrA.

<p>The naïve T cells isolated from rat spleen were cultured with or without PrA (20 nM) for 72 h. A chemotactic migration assay was used to assess the migration of naïve T cells in the presence or absence of PrA towards different doses of either recombinant IP-10 or Mig. (A) PrA-conditioned T cells exhibited decreased migration in presence of 25 ng/mL of IP-10, but not at 50 ng/mL or 100 ng/mL, compared with those of non-condition T cells. (B) The migration of PrA-conditioned T cells was decreased at 50 ng/mL and 100 ng/mL of Mig, but not at 200 ng/mL, as compared with those of non-conditioned T cells. The result suggests that the capacity of T cell migration was partially affected by PrA <i>in vitro</i>. * indicates <i>p</i><0.05, and bars indicate comparators.</p

PrA conditioning reduced PBMC IP-10 secretion <i>in vitro</i>.

<p>PBMCs isolated from control recipient rats on day four were cultured with different doses of PrA for 72(n = 3 per group). (A) PBMC viability was measured by MTT assay. The highest dose induced a significant decrease in viable cell count, therefore, only 5 nM and 20 nM concentrations were used in subsequent experiments. (B) Culture supernatants of PBMC with or without PrA condition were harvested and analyzed for the production of IP-10 by ELISA. * indicates <i>p</i><0.05 when comparing treatment condition to control.</p

PrA prevented CXCR3⁺T cell infiltration into allografts.

<p>(A) The heart allograft was harvested on day seven post heart transplantation, sectioned, and stained for TCR (TMRITC, red) and CXCR3 (FITC, green). The extent of colocalization (yellow) of TCR (T cell marker) and CXCR3 indicating CXCR3⁺ T cell infiltration into allografts was significantly reduced after PrA administration. The results are representative of three independent experiments. (B) The relative quantitative analysis to determine the percentage of CXCR3⁺TCR⁺ cells within infiltrating cells of allografts further showed that PrA treatment inhibited the CXCR3⁺ T cell infiltration into allografts. *indicates <i>p</i><0.05 when comparing treatment to control.</p