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We attempt to reduce the computational costs in vision transformers (ViTs), which increase quadratically in the token number. We present a novel training paradigm that trains only one ViT model at a time, but is capable of providing improved image recognition performance with various computational costs. Here, the trained ViT model, termed super vision transformer (SuperViT), is empowered with the versatile ability to solve incoming patches of multiple sizes as well as preserve informative tokens with multiple keeping rates (the ratio of keeping tokens) to achieve good hardware efficiency for inference, given that the available hardware resources often change from time to time. Experimental results on ImageNet demonstrate that our SuperViT can considerably reduce the computational costs of ViT models with even performance increase. For example, we reduce 2 × FLOPs of DeiT-S while increasing the Top-1 accuracy by 0.2% and 0.7% for 1.5 × reduction. Also, our SuperViT significantly outperforms existing studies on efficient vision transformers. For example, when consuming the same amount of FLOPs, our SuperViT surpasses the recent state-of-the-art EViT by 1.1% when using DeiT-S as their backbones. The project of this work is made publicly available at https://github.com/lmbxmu/SuperViT. [ABSTRACT FROM AUTHOR]

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]

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease characterized by persistent airflow limitation but still lacking effective treatments. Perilla frutescens (L.) Britt. , an important traditional medicinal plant with excellent antioxidant and anti-inflammatory properties, is widely used for the treatment of respiratory disease in China. However, its protective activity and mechanism against COPD airway inflammation have not been fully studied. Here, the anti-inflammatory effects of the PLE were investigated, and its underlying mechanisms were then elucidated. The presented results suggested a notable effect of the PLE on airway inflammation of COPD, by significantly ameliorating inflammatory cell infiltration in lung tissue, lessening leukocytes (lymphocytes, neutrophils, and macrophages) and inflammatory mediators (interleukin 4 (IL-4), IL-6, IL-17A, interferon γ (IFN-γ), and tumor necrosis factor α (TNF-α)) in the bronchoalveolar lavage fluid (BALF) of cigarette smoke (CS)/lipopolysaccharide (LPS)-induced COPD mice in vivo and inhibiting the production of inflammatory factors (nitric oxide (NO), IL-6, and TNF-α) and intracellular reactive oxygen species (ROS) in LPS-stimulated RAW264.7 cells in vitro. For further extent, PLE treatment significantly suppressed the expression and phosphorylation of TLR4, Syk, PKC, and NF-κB p65 in vivo and their mRNA in vitro. Subsequently, by co-treating with their inhibitors in vitro , its potential mechanism via TLR4/Syk/PKC/NF-κB p65 signals was disclosed. In summary, the obtained results indicated a noteworthy effective activity of the PLE on COPD inflammation, and partly, the TLR4/Syk/PKC/NF-κB p65 axis might be the potential mechanism. [ABSTRACT FROM AUTHOR]

Introduction: Asthma–chronic obstructive pulmonary (COPD) overlap (ACO) coexists with asthma and COPD syndrome characteristics, with more frequent exacerbations, heavier disease burden, higher medical utilization, and even lower quality of life. However, the ACO standard medications supported by evidence-based medicine have not yet appeared. Methods: By using an ACO mouse model established previously and LPS-stimulated RAW264.7 macrophages in vitro, a potential therapeutic candidate, EAPP-2, was screened from derivatives of 3-arylbenzofuran, and its effect and mechanism on ACO inflammation were evaluated. Results: EAPP-2 significantly alleviated airway inflammation in ACO mice and also inhibited the inflammatory reactions in LPS-induced RAW264.7 macrophages in vitro. Furthermore, EAPP-2 significantly inhibited the expression and phosphorylation of spleen tyrosine kinase (Syk), a common target regulating both eosinophils and neutrophils inflammation. In addition to this, EAPP-2 significantly down-regulates the expression of NF-κB, p-NF-κB, and NLRP3 in vivo and in vitro. Moreover, by using specific inhibitors in vitro, it was validated that EAPP-2 targeted on Syk and then regulated its downstream NF-κB and NLRP3. Conclusion: EAPP-2 is shown to be a potentially useful therapeutic candidate for ACO, and its mechanism is at least partially achieved by targeting on Syk and then inhibiting NF-κB or NLRP3. Moreover, this study suggests that Syk may be a potentially effective target for ACO therapy. [ABSTRACT FROM AUTHOR]

Background: Perilla frutescens (L.) Britt., a classic medicinal plant, has been demonstrated to have anti-inflammatory and anti-allergic effects in asthma. Perilla leaves extract (PLE) exerted significant therapeutic effect against allergic asthma inflammation through Syk inhibition. But the active chemical ingredients from PLE are complex and unclear, it is difficult to fully elucidate its pharmacological mechanisms. Methods: A method was established for rapid screening and characterization of active ingredients from PLE that targeted Syk, with which three potential active ingredients were identified. By using OVA-induced allergic asthma mouse model in vivo, OVA-induced human PBMCs inflammation model and DNP-IgE/BSA-induced RBL-2H3 cells model in vitro, the effects and mechanisms of PLE and its active components were evaluated. Results: Using Syk-affinity screening method, roseoside (RosS), vicenin-2 (Vic-2) and rosmarinic acid (RosA) were identified from PLE. In vitro, PLE and its ingredients showed significant inhibitory activities against Syk, with their mixture (Mix, prepared by RosS, Vic-2 and RosA in accordance with their ratio in Syk-conjugated beads bound fraction) showing a stronger inhibitory activity. RosS, Vic-2 and RosA also showed significant effects on allergic asthma, and a synergistic effect of Mix was observed. Moreover, treatment with PLE, RosS, Vic-2, RosA, and Mix significantly inhibited the expression and phosphorylation of Syk, PKC, NF-κB p65, and cPLA2 in allergic mice lung tissue and in RBL-2H3 cells. Conclusion: PLE may alleviate allergic airway inflammation partly through the multiple components synergistic targeting on Syk and its downstream inflammatory pathway. [ABSTRACT FROM AUTHOR]

Online image hashing has attracted increasing research attention recently, which receives large-scale data in a streaming manner to update the hash functions on-the-fly. Its key challenge lies in the difficulty of balancing the learning timeliness and model accuracy. To this end, most works follow a supervised setting, i.e., using class labels to boost the hashing performance, which defects in two aspects: first, strong constraints, e.g., orthogonal or similarity preserving, are used, which however are typically relaxed and lead to large accuracy drops. Second, large amounts of training batches are required to learn the up-to-date hash functions, which largely increase the learning complexity. To handle the above challenges, a novel supervised online hashing scheme termed Hadamard Matrix Guided Online Hashing (HMOH) is proposed in this paper. Our key innovation lies in introducing Hadamard matrix, which is an orthogonal binary matrix built via Sylvester method. In particular, to release the need of strong constraints, we regard each column of Hadamard matrix as the target code for each class label, which by nature satisfies several desired properties of hashing codes. To accelerate the online training, LSH is first adopted to align the lengths of target code and to-be-learned binary code. We then treat the learning of hash functions as a set of binary classification problems to fit the assigned target code. Finally, extensive experiments on four widely-used benchmarks demonstrate the superior accuracy and efficiency of HMOH over various state-of-the-art methods. Codes can be available at https://github.com/lmbxmu/mycode. [ABSTRACT FROM AUTHOR]

Online image hashing aims to update hash functions on-the-fly along with newly arriving data streams, which has found broad applications in computer vision and beyond. To this end, most existing methods update hash functions simply using discrete labels or pairwise similarity to explore intra-class relationships, which, however, often deteriorates search performance when facing a domain gap or semantic shift. One reason is that they ignore the particular semantic relationships among different classes, which should be taken into account in updating hash functions. Besides, the common characteristics between the label vectors (can be regarded as a sort of binary codes) and to-be-learned binary hash codes have left unexploited. In this paper, we present a novel online hashing method, termed Similarity Preserving Linkage Hashing (SPLH), which not only utilizes pairwise similarity to learn the intra-class relationships, but also fully exploits a latent linkage space to capture the inter-class relationships and the common characteristics between label vectors and to-be-learned hash codes. Specifically, SPLH first maps the independent discrete label vectors and binary hash codes into a linkage space, through which the relative semantic distance between data points can be assessed precisely. As a result, the pairwise similarities within the newly arriving data stream are exploited to learn the latent semantic space to benefit binary code learning. To learn the model parameters effectively, we further propose an alternating optimization algorithm. Extensive experiments conducted on three widely-used datasets demonstrate the superior performance of SPLH over several state-of-the-art online hashing methods. [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]

Background. Henoch–Schönlein purpura nephritis (HSPN) is the principal cause of morbidity and mortality in Henoch–Schönlein purpura (HSP). However, there is no absolute consensus for the best management of severe HSPN till now. Qingzixiaoban Granule (QZXB GR), a traditional Chinese medicine formula, has been applied to treat HSP in clinical in China. However, the therapeutic effects and potential mechanism of QZXB GR on HSPN is still unknown. Methods. A Gliadin plus Indian Ink-induced HSPN mice model was established. Renal histopathologic changes and the subcutaneous hemorrhage on left legs were assessed. Hematuria and proteinuria were determined using hemocytometer and bicinchoninic acid assay, respectively. The serum circular immune complex and interleukin-6 were quantified by ELISA. Using blood biochemical analyzer, the renal biochemical parameters, including serum total protein, albumin, creatinine, and blood urea nitrogen, were measured. The deposition of immune complex in renal tissues and the lymphocyte subsets in peripheral blood and spleen was investigated by immunohistochemistry and flow cytometry. Results. QZXB GR treatment significantly ameliorated renal injury in HSPN mice, by attenuating renal histopathological changes, reducing subcutaneous hemorrhage, decreasing proteinuria/hematuria, regulating renal biochemical parameters, and inhibiting the release of serum interleukin-6. Furthermore, QZXB GR treatment significantly decreased the level of serum circular immune complex, decreased immune complex IgA and IgG deposition in renal tissue, and suppressed Th2 immunodeviation. Conclusion. QZXB GR could prevent renal injury in HSPN mice, and its renoprotective mechanism might be exerted partly through suppressing immune complexes deposition and Th2 immune deviation. [ABSTRACT FROM AUTHOR]

Amurensin H, a resveratrol dimer derived from Vitis amurensis Rupr, has several biological effects, including anti-inflammatory and antioxidant activities. Studies have found that amurensin H attenuated asthma-like allergic airway inflammation. However, its protective activity on chronic obstructive pulmonary disease (COPD) airway inflammation is not fully explored. The present study used a lipopolysaccharide (LPS)/cigarette smoke–induced mice model and an LPS-stimulated THP-1–derived macrophages model to measure the lung tissue's morphology changes. The results showed that amurensin H ameliorated the histological inflammatory alterations in the lung tissues, leading to a decrease in the expression of interleukin 6 (IL-6), IL-17A, tumor necrosis factor α (TNF-α), and interferon γ in bronchoalveolar lavage fluid. Amurensin H also significantly inhibited the release of IL-1β, IL-6, IL-8, and TNF-α in LPS-stimulated THP-1–derived macrophages. Furthermore, amurensin H markedly inhibited the expressions of p-Syk, nuclear factor κB (NF-κB), and p-NF-κB both in vivo and in vitro. Results from cotreatment with Syk inhibitor BAY61-3606 and NF-κB inhibitor BAY11-7082 in vitro revealed that amurensin H's protective effect against airway inflammation could be due partly to the inhibition of the Syk/NF-κB pathway. These findings suggest that amurensin H shows therapeutic effects on COPD airway inflammation, and inhibiting the Syk/NF-κB pathway might be part of its underlying mechanisms. [ABSTRACT FROM AUTHOR]

Methylophiopogonanone A (MO-A), an active homoisoflavonoid of the Chinese herb Ophiopogon japonicus which has been shown to have protective effects on cerebral ischemia/reperfusion (I/R) injury, has been demonstrated to have anti-inflammatory and anti-oxidative properties. However, little is known about its role in cerebral I/R injury. Therefore, in this study, by using a middle cerebral artery occlusion (MCAO) and reperfusion rat model, the effect of MO-A on cerebral I/R injury was examined. The results showed that MO-A treatment reduced infarct volume and brain edema, improved neurological deficit scores, reversed animal body weight decreases, and increased animal survival time in the stroke groups. Western blotting showed that MO-A suppressed MMP-9, but restored the expression of claudin-3 and claudin-5. Furthermore, transmission electron microscopy were monitored to determine the blood–brain barrier (BBB) alterations in vitro. The results showed that MO-A markedly attenuated BBB damage in vitro. Additionally, MO-A inhibited ROS production in ECs and MMP-9 release in differentiated THP-1 cells in vitro, and suppressed ICAM-1 and VCAM-1 expression in ECs and leukocyte/EC adhesion. In conclusion, our data indicate that MO-A has therapeutic potential against cerebral I/R injury through its ability to attenuate BBB disruption by regulating the expression of MMP-9 and tight junction proteins. [ABSTRACT FROM AUTHOR]

To identify quantitative trait loci (QTLs) for flower-related characters in Luffa, a genetic map was constructed by using 110 F individuals derived from interspecific hybrids between Luffa acutangula Roxb. (inbred line '28-0-0') and L. cylindrica Roem. (inbred line '37-0-1-1'). A total of 258 sequence-related amplified polymorphism markers were mapped on 24 linkage groups, spanning 822.86 cM, with a mean marker interval of 3.49 cM. Then, 23 QTLs were identified through composite interval mapping, and included nine, eight and six for first female flower node, male flower diameter and flowering time, respectively. Importantly, the above QTLs individually explained 0.03-24.61 % of total phenotypic variance of the corresponding trait. These findings provide a basis for molecular marker assisted breeding in Luffa. [ABSTRACT FROM AUTHOR]

Chlorogenic acid (CGA) is found in many plants that are used as medicinal substances in traditional Chinese medicine injectables (TCMIs). However, to date, there is controversy as to whether CGA is the major cause of TCMIs-related hypersensitivity administered intravenously. Therefore, the aim of this study was to evaluate the potential sensitization of CGA and structure–activity differences between its isomers using an intravenous exposure mouse model. The results showed that popliteal lymph nodes proliferation was significantly induced by CGA and its isomers. Both CGA and isochlorogenic acid A (iso-CGA A) significantly enhanced the secretion of trinitrophenyl (TNP) ovalbumin-specific immunoglobulin (Ig)G1; and iso-CGA B significantly induced TNP-specific IgG1, IgM, and IgG2b secreting. Furthermore, the results of quantitative structure–activity relationship analysis suggested that chemical structure factors, including atomic mass, electronegativity, atom shape and size, atom distribution, atomic weight, and atomic polarizabilities, the ionic currents, were significantly correlated with the potential sensitization of CGA and its isomers. In summary, when administered intravenously, the strength and type of sensitization may be correlated with structure differences in the CGA family. [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]

Brusatol derivative-34 (Bru-34), a derivative of brusatol, has been shown significantly anti-inflammatory activity in mice in our previously work. However, to our knowledge, there were very limited studies on how Bru-34 affected airway inflammation. Thus, in this present study, the effects and potential mechanisms of Bru-34 on allergic airway inflammation were examined both in vivo and in vitro. The results showed that Bru-34 attenuated the allergic airway inflammation in mice, with significant decreasing of the inflammatory cells and mediators in bronchoalveolar lavage fluids and attenuation of the histopathological alterations in the lung tissues. In addition, Bru-34 significantly inhibited the release of inflammatory cytokines in antigen induced rat basophilic leukemia -2H3 (RBL-2H3) cells. What's more, Bru-34 significantly decreased the expression of spleen tyrosine kinase (Syk), p -Syk, cytoplasmic phospholipase A2 (cPLA2), p -cPLA2, nuclear factor-κB (NF-κB) and p-NF-κB both in allergic mice lung tissue and antigen induced RBL-2H3 cells. Furthermore, the collaborative effects of Bru-34 with inhibitors against Syk, cPLA2, and NF-κB, showed that Syk was an important target of Bru-34, and cPLA2 and NF-κB played important roles in the coordinated inflammatory response. In conclusion, Bru-34 could significantly modulate the allergic airway inflammation, and its potential mechanism was revealed at least partially via down-regulating of Syk-cPLA2 -NF-κB signaling. [ABSTRACT FROM AUTHOR]