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Online image hashing has received increasing research attention recently, which processes large-scale data in a streaming fashion to update the hash functions on-the-fly. To this end, most existing works exploit this problem under a supervised setting, i.e., using class labels to boost the hashing performance, which suffers from the defects in both adaptivity and efficiency: First, large amounts of training batches are required to learn up-to-date hash functions, which leads to poor online adaptivity. Second, the training is time-consuming, which contradicts with the core need of online learning. In this paper, a novel supervised online hashing scheme, termed Fast Class-wise Updating for Online Hashing (FCOH), is proposed to address the above two challenges by introducing a novel and efficient inner product operation. To achieve fast online adaptivity, a class-wise updating method is developed to decompose the binary code learning and alternatively renew the hash functions in a class-wise fashion, which well addresses the burden on large amounts of training batches. Quantitatively, such a decomposition further leads to at least 75 percent storage saving. To further achieve online efficiency, we propose a semi-relaxation optimization, which accelerates the online training by treating different binary constraints independently. Without additional constraints and variables, the time complexity is significantly reduced. Such a scheme is also quantitatively shown to well preserve past information during updating hashing functions. We have quantitatively demonstrated that the collective effort of class-wise updating and semi-relaxation optimization provides a superior performance comparing to various state-of-the-art methods, which is verified through extensive experiments on three widely-used datasets. [ABSTRACT FROM AUTHOR]

The low‐grade, chronic inflammation initiated by TLR4‐triggered innate immune responses has a central role on early osteoarthritis. Amurensin H is a resveratrol dimer with anti‐inflammatory and anti‐apoptotic effects, while its effects on TLR‐4 signals to inhibit osteoarthritis are still unclear. In the present study, treatment with amurensin H for 2 weeks in monosodium iodoacetate‐induced mice significantly slows down cartilage degeneration and inflammation using macroscopic evaluation, haematoxylin and eosin (HE) staining and micro‐magnetic resonance imaging. In IL‐1β‐stimulated rat chondrocytes, amurensin H suppresses the production of inflammatory mediators including nitric oxide, IL‐6, IL‐17, PGE2 and TNF‐α using Greiss and ELISA assay. Amurensin H inhibits matrix degradation via decreasing levels of MMP‐9 and MMP‐13 using Western blot assay, promotes synthesis of type II collagen and glycosaminoglycan using immunostaining and safranin O staining, respectively. Amurensin H inhibits intracellular and mitochondrial reactive oxygen species (ROS) generation, and mitochondrial membrane depolarization using DCFH‐DA, MitoSOX Red and JC‐1 assay as well. IL‐1β stimulates TLR4 activation and Syk phosphorylation in chondrocytes, while amurensin H inhibits TLR4/Syk signals and downstream p65 phosphorylation and translocation in a time and dose‐dependent manner. Together, these results suggest that amurensin H exerts chondroprotective effects by attenuating oxidative stress, inflammation and matrix degradation via the TLR4/Syk/NF‐κB pathway. [ABSTRACT FROM AUTHOR]

ABSTRACT Immune-mediated drug hypersensitivity is a particularly concerning health-safety issue among clinicians given its unpredictability and potentially life-threatening effects, especially with exposure to intravenous drugs. Therefore, the development of intravenous drug-exposure models for drug-hazard assessments has garnered increasing interest in recent years. In this study, we used reporter antigens popliteal lymph node assay to investigate the potential value of intravenous exposure to a selected variety of allergenic compounds, including ovalbumin (OVA), concanavalin A (ConA) and diclofenac. The trinitrophenyl (TNP)-specific antibody-forming cells were used to assess the systemic immune responses to a bystander antigen. Mice were subsequently sensitized by TNP-OVA, and then intravenous exposure to one of the selective compounds. As expected, all positive compounds induced significant popliteal lymph node (PLN) proliferation compared with the control. OVA significantly increased Cluster of Differentiation 4 receptors (CD4)+ interleukin-4 (IL-4)+ T-helper 2 (Th2) cells and, consequently, increased the ratios of IL-4/interferon- γ (IFN- γ) antibody-forming cells (AFCs) in PLNs, while bringing about a dose-dependent increase in immunoglobulin G1 (IgG1) AFCs; these findings indicate that a Th2 hypersensitivity response was induced. A Th2 response was also observed in diclofenac sodium-treated groups, and for ConA, a more mixed Th1/Th2 immune response appeared to be induced. In addition, there was no marked reaction with the negative compound. Together, it seems likely that the intravenous exposure model may be useful for drug-induced systemic hypersensitivity assessments. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]