Image recoloring detection based on inter-channel correlation

Image recoloring is an emerging editing technique that can change the color style of an image by modifying pixel values.With the rapid proliferation of social networks and image editing techniques, recolored images have seriously hampered the authenticity of the communicated information.However, there are few works specifically designed for image recoloring.Existing recoloring detection methods still have much improvement space in conventional recoloring scenarios and are ineffective in dealing with hand-crafted recolored images.For this purpose, a recolored image detection method based on inter-channel correlation was proposed for conventional recoloring and hand-crafted recoloring scenarios.Based on the phenomenon that there were significant disparities between camera imaging and recolored image generation methods, the hypothesis that recoloring operations might destroy the inter-channel correlation of natural images was proposed.The numerical analysis demonstrated that the inter-channel correlation disparities can be used as an important discriminative metric to distinguish between recolored images and natural images.Based on such new prior knowledge, the proposed method obtained the inter-channel correlation feature set of the image.The feature set was extracted from the channel co-occurrence matrix of the first-order differential residuals of the differential image.In addition, three detection scenarios were assumed based on practical situations, including scenarios with matching and mismatching between training-testing data, and scenario with hand-crafted recoloring.Experimental results show that the proposed method can accurately identify recolored images and outperforms existing methods in all three hypothetical scenarios, achieving state-of-the-art detection accuracy.In addition, the proposed method is less dependent on the amount of training data and can achieve fairly accurate prediction results with limited training data

Reporting, presentation and wording of recommendations in clinical practice guideline for gout: a systematic analysis

OBJECTIVES: We systematically analysed recommendations from gout guidelines as an example, to provide a basis for developing a reporting standard of recommendations in clinical practice guidelines (CPGs). DESIGN: Systematic review without meta-analysis. METHODS: We systematically searched MEDLINE and all relevant guideline websites (National Institute for Health and Care Excellence, National Guideline Clearinghouse, Scottish Intercollegiate Guidelines Network, WHO, Guidelines International Network, DynaMed, UpTodate, Best Practice) from their inception to January 2017 to identify and select gout CPGs. We used search terms such as 'gout', 'hyperuricemia' and 'guideline'. We included the eligible CPGs of gout according to the predefined inclusion and exclusion criteria after screening titles, abstracts and full texts. The characteristics of recommendations reported in the included guidelines were extracted and analysed

STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.

One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection

HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection

<div><p>Enterovirus 71 (EV71) is an RNA virus that causes hand-foot-mouth disease (HFMD), and even fatal encephalitis in children. Although EV71 pathogenesis remains largely obscure, host immune responses may play important roles in the development of diseases. Recognition of pathogens mediated by Toll-like receptors (TLRs) induces host immune and inflammatory responses. Intracellular TLRs must traffic from the endoplasmic reticulum (ER) to the endolysosomal network from where they initiate complete signaling, leading to inflammatory response. This study reveals a novel mechanism underlying the regulation of TLR7 signaling during EV71 infection. Initially, we show that multiple cytokines are differentially expressed during viral infection and demonstrate that EV71 infection induces the production of proinflammatory cytokines through regulating TLR7-mediated p38 MAPK, and NF-κB signaling pathways. Further studies reveal that the expression of the endosome-associated protein hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) is upregulated and highly correlated with the expression of TLR7 in EV71 infected patients, mice, and cultured cells. Virus-induced HRS subsequently enhances TLR7 complex formation in early- and late-endosome by interacting with TLR7 and TAB1. Moreover, HRS is involved in the regulation of the TLR7/NF-κB/p38 MAPK and the TLR7/NF-κB/IRF3 signaling pathways to induce proinflammatory cytokines and interferons, respectively, resulting in the orchestration of inflammatory and immune responses to the EV71 infection. Therefore, this study demonstrates that HRS acts as a key component of TLR7 signaling to orchestrate immune and inflammatory responses during EV71 infection, and provides new insights into the mechanisms underlying the regulation of host inflammation and innate immunity during EV71 infection.</p></div

The sub-cellular localization of HRS during TLR7 signaling activation.

<p><b>(A–G)</b> Macrophages were stimulated without or with R848 for 15 min, and then probed with HRS or organelles markers antibodies against clathrin (<b>A</b>), EEA1 (<b>B</b>), Rab7 (<b>C</b>), Rab11 (<b>D</b>), LAMP1 (<b>E</b>), Calnexin (<b>F</b>) or Rcas1 (<b>G</b>) before confocal microscopy, Bar = 20 μm. <b>(H)</b> The intensity of colocalization was calculated by using Image J software analysis. +++, >80% colocalization; ++, 60%~80% colocalization; +, 40%~60% colocalization; -, < 40% colocalization.</p