Rechargeable batteries with organic electrodes are preferred to those with transition-metal-containing electrodes for their environmental friendliness, and resource availability, but all such batteries reported to date are based on organic electrolytes, which raise concerns of safety and performance. Here an aqueous-electrolyte all-organic rechargeable battery is reported, with a maximum operating voltage of 2.1 V, in which polytriphenylamine (PTPAn) and 1,4,5,8-naphthalenetetracarboxylic dianhydride (NTCDA)-derived polyimide (PNTCDA) serve as cathode and anode material, respectively. A key feature of the design is use of a "water-in-salt" electrolyte to bind "free" water; this impedes the side reaction of water oxidation, thereby enabling excellent reversibility in aqueous solution. The battery can deliver a maximum energy density of 52.8 Wh kg , which is close to most of the all-organic batteries with organic electrolytes. The battery exhibits a supercapacitor-like high power of 32 000 W kg and a long cycle life (700 cycles with capacity retention of 85 %), due to the kinetics not being limited by ion diffusion at either electrode.

Computing discrete geodesic distance over triangle meshes is one of the fundamental problems in computational geometry and computer graphics. In this problem, an effective window pruning strategy can significantly affect the actual running time. Due to its importance, we conduct an in-depth study of window pruning operations in this paper, and produce an exhaustive list of scenarios where one window can make another window partially or completely redundant. To identify a maximal number of redundant windows using such pairwise cross checking, we propose a set of procedures to synchronize local window propagation within the same triangle by simultaneously propagating a collection of windows from one triangle edge to its two opposite edges. On the basis of such synchronized window propagation, we design a new geodesic computation algorithm based on a triangle-oriented region growing scheme. Our geodesic algorithm can remove most of the redundant windows at the earliest possible stage, thus significantly reducing computational cost and memory usage at later stages. In addition, by adopting triangles instead of windows as the primitive in propagation management, our algorithm significantly cuts down the data management overhead. As a result, it runs 4-15 times faster than MMP and ICH algorithms, 2-4 times faster than FWP-MMP and FWP-CH algorithms, and also incurs the least memory usage.Due to the aforementioned importance, we conduct an in-depth study of window pruning operations in this paper. If we focus on

IntroductionAbnormal toll-like receptor (TLR)3 signaling plays an indispensable role in pathogenesis of both experimental and human rheumatoid arthritis, and microRNAs (miRNAs) might orchestrate this signaling pathway. This study was performed to determine the relationship between miR-26a and TLR3 in rat macrophages and to observe effects of miR-26a mimic on pristane induced arthritis (PIA) in rats.MethodsDual luciferase reporter assay was used to validate the direct interaction between miR-26a (a candidate miRNA to target tlr3 mRNA) and tlr3 3′UTR. MiR-26a regulation on TLR3 gene expression was determined using RT-qPCR and Western blotting after miR-26a mimics and inhibitors were transfected into rat macrophage line NR8383 cells. Poly I:C (TLR3 ligand) was used to trigger TLR3 activation, and mRNA expression of its downstream cytokines interferon (ifn)-β and tumor necrosis factor (tnf)-α was accordingly detected to determine the regulation of TLR3 signaling. Expressions of TLR3 and miR-26a were detected during rat bone marrow derived macrophage (BMDM) induction, in pristane stimulated NR8383 cells and spleens from methotrexate (MTX) treated PIA rats. A miR-26a mimic was administrated intraperitoneally to PIA rats, and arthritis severity was evaluated by macroscopic or microscopic observations.ResultsDirect target relationship between miR-26a and tlr3 mRNA in rats was confirmed. Modifications of miR-26a function by transfection of miR-26a mimics and inhibitors exhibited corresponding repression and augmentation of TLR3 and its signaling downstream cytokine expressions in NR8383 cells. The alteration of miR-26a expression was negatively related with TLR3 expression during BMDM induction, in pristane-primed NR8383 cells and PIA rat spleens. Moreover, both abnormal expressions were rescued in MTX treated arthritis rat spleens. The miR-26a mimic treatment displayed the depression of TLR3 expression and ameliorated the disease severity in the rats with pristane induced arthritis.ConclusionsMiR-26a negatively regulates TLR3 signaling via targeting of TLR3 itself in rat macrophages, and this finding provides a novel insight into abnormal TLR3 overexpression during experimental arthritis.

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Abstract-Subspace clustering aims to partition the data points drawn from a union of subspaces according to their underlying subspaces. For accurate semisupervised subspace clustering, all data that have a must-link constraint or the same label should be grouped into the same underlying subspace. However, this is not guaranteed in existing approaches. Moreover, these approaches require additional parameters for incorporating supervision information. In this paper, we propose a constrained low-rank representation (CLRR) for robust semisupervised subspace clustering, based on a novel constraint matrix constructed in this paper. While seeking the low-rank representation of data, CLRR explicitly incorporates supervision information as hard constraints for enhancing the discriminating power of optimal representation. This strategy can be further extended to other state-of-the-art methods, such as sparse subspace clustering. We theoretically prove that the optimal representation matrix has both a block-diagonal structure with clean data and a semisupervised grouping effect with noisy data. We have also developed an efficient optimization algorithm based on alternating the direction method of multipliers for CLRR. Our experimental results have demonstrated that CLRR outperforms existing methods.

MicroRNA-21 (miR-21), probably one of the most studied miRNAs to date, is found pleiotropic in various biological events. Its emerging role in pulmonary remodeling has attracted extensive attention. This review summarizes the genomic information of its primary transcript and various transcriptional regulations on its promoter. In addition, the role of miR-21 in pulmonary remodeling related signaling such as transforming growth factor β (TGF-β), bone morphogenetic protein (BMP), epidermal growth factor receptor (EGFR) and Notch signaling is discussed. Various validated miR-21 target genes participate in controlling of the overactive cell accumulation, smooth muscle contraction, inflammatory stress (trigger for lung epithelium damage), extracellular matrix deposition and hypoxia-induced disorders. Moreover, we focus on its particular implication in events including inflammatory stress-driven epithelium damage, epithelial-to-mesenchymal transition (EMT), transdifferentiation of fibroblasts into myofibroblasts, hypoxia stimuli and ROS response, as well as some other pulmonary remodeling related events such as overactive fibroblast (myofibroblast) accumulation, extracellular matrix deposition, and angiogenesis. Here, we summarize the strong potential of miR-21 in pulmonary remodeling and provide novel clues for further research in this area.

In recent times, image inpainting has witnessed rapid progress due to the generative adversarial networks (GANs) that are able to synthesize realistic contents. However, most existing GAN-based methods for semantic inpainting apply an auto-encoder architecture with a fully connected layer, which cannot accurately maintain spatial information. In addition, the discriminator in existing GANs struggles to comprehend highlevel semantics within the image context and yields semantically consistent content. Existing evaluation criteria are biased toward blurry results and cannot well characterize edge preservation and visual authenticity in the inpainting results. In this paper, we propose an improved GAN to overcome the aforementioned limitations. Our proposed GAN-based framework consists of a fully convolutional design for the generator which helps to better preserve spatial structures and a joint loss function with a revised perceptual loss to capture high-level semantics in the context. Furthermore, we also introduce two novel measures to better assess the quality of image inpainting results. The experimental results demonstrate that our method outperforms the state-of-the-art under a wide range of criteria.

Matrilin-1 (Matn1), a cartilage-specific peri-cellular and extracellular matrix (ECM) protein, has been hypothesized to regulate ECM interactions and transmit mechanical signals in cartilage. Since Matn1 knock-out (Matn1-/-) mice exhibit a normal skeleton, its function in vivo is unclear. In this study, we found that the anabolic Acan and Col2a transcript levels were significantly higher in wildtype (Matn1+/+) mouse cartilage than that of MATN1-/- mice in vivo. However, such difference was not observed between Matn1+/+ and MATN1-/- chondrocytes cultured under stationary conditions in vitro. Cyclic loading significantly stimulated Acan and Col2a transcript levels in Matn1+/+ but not in MATN1-/- chondrocytes. This suggests that, while Matn1+/+ chondrocytes increase their anabolic gene expression in response to mechanical loading, the MATN1-/- chondrocytes fail to do so because of the deficiency in mechanotransduction. We also found that altered elastic modulus of cartilage matrix in Matn1-/- mice, suggesting the mechanotransduction has changed due to the deficiency of Matn1. To understand the impact of such deficiency on joint disease, mechanical loading was altered in vivo by destabilization of medial meniscus. While Matn1+/+ mice exhibited superficial fissures and clefts consistent with mechanical damage to the articular joint, Matn1-/- mice presented more severe cartilage lesions characterized by proteoglycan loss and disorganization of cells and ECM. This suggests that Matn1 deficiency affects pathogenesis of post-traumatic osteoarthritis by failing to up-regulate anabolic gene expression. This is the first demonstration of Matn1 function in vivo, which suggests its protective role in cartilage degeneration under altered mechanical environment.