style loss and content loss. However, such pre-trained networks are originally designed for object recognition, and hence the high-level features o en focus on the primary target and neglect other details. As a result, when input images contain multiple objects potentially at di erent depths, the resulting images are o en unsatisfactory because image layout is destroyed and the boundary between the foreground and background as well as di erent objects becomes obscured. We observe that the depth map e ectively re ects the spatial distribution in an image and preserving the depth map of the content image a er stylization helps produce an image that preserves its semantic content. In this paper, we introduce a novel approach for neural style transfer that integrates depth preservation * Corresponding author's email: cmm@nankai.edu.cn Permission to make digital or hard copies of all or part of this work for personal or classroom use is granted without fee provided that copies are not made or distributed for pro t or commercial advantage and that copies bear this notice and the full citation on the rst page. Copyrights for components of this work owned by others than the author(s) must be honored. Abstracting with credit is permi ed. To copy otherwise, or republish, to post on servers or to redistribute to lists, requires prior speci c permission and/or a fee.

Since its inception in 2015, Style Transfer has focused on texturing a content image using an art exemplar. Recently, the geometric changes that artists make have been acknowledged as an important component of style [42,55,62,63]. Our contribution is to propose a neural network that, uniquely, learns a mapping from a 4D array of inter-feature distances to a non-parametric 2D warp field. The system is generic in not being limited by semantic class, a single learned model will suffice; all examples in this paper are output from one model.Our approach combines the benefits of the high speed of Liu et al. [42] with the non-parametric warping of Kim et al. [55]. Furthermore, our system extends the normal NST paradigm: although it can be used with a single exemplar, we also allow two style exemplars: one for texture and another for geometry. This supports far greater flexibility in use cases than single exemplars can provide.

Aim:To investigate the effect of balsalazine treatment on intestinal mucosal permeability in dextran sulfate sodium (DSS)-induced colitis and to determine the mechanism of the balsalazine-induced changes. Methods: Experimental colitis was induced in C57BL/6J mice by the administration of 5% DSS. Balsalazine was administered intragastrically at doses of 42, 141, and 423 mg/kg. The disease activity index (DAI) score was evaluated and colon tissue was collected for the assessment of histological changes. The amount of malondialdehyde (MDA) in the colon was determined, along with the activity of myeloperoxidase (MPO), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Mucosa from the small intestine was collected to determine the levels of tumor necrosis factor (TNF)-α and interferon (IFN)-γ. The mucosa was ultrastructurally examined with transmission electron microscopy and intestinal permeability was assayed using Evans blue. Results: Balsalazine was found to reduce the DAI score and the histological index (HI) score, decrease the MDA content and the activity of MPO, and increase the activity of SOD and GSH-Px in colitis mice. At the same time, balsalazine ameliorated microvillus and tight junction structure, resulting in a decrease in the amount of Evans blue permeating into the intestinal wall and the levels of TNF-α and IFN-γ in colitis mice. Conclusion: In colitis mice, the anti-colitis effect of balsalazine results in a decrease in intestinal mucosal permeability. The mechanism of this effect is partly associated with balsalazine's antioxidative and anti-inflammatory effects.

Molybdenum disulfide (MoS 2 ) has excellent photothermal conversion abilities, an ultra-high specific surface area, and has been extensively explored for use in biomedicine. However, the high toxicity associated with MoS 2 has limited its biological applications for in vivo photothermal therapy and drug delivery systems. Herein, we have developed cationic hydroxyethyl cellulose (JR400) surface-modified MoS 2 nanoparticles (NPs) that are responsive to near-infrared (NIR) laser irradiation as a transdermal drug delivery system (TDDS). Herein, we confirmed the preparation of hexagonal phase MoS 2 with robust surface modification with JR400. The flower-like morphology of the NPs had an average diameter of 355 ± 69.3 nm limiting the absorption of the NPs through the stratum corneum. With the ability to efficiently load 90.4 ± 0.3% of the model drug atenolol (ATE), where 1 g of JR400-MoS 2 NPs was able to load 3.6 g ATE, we assayed the controlled release capacity in vitro skin penetration studies. These JR400-MoS 2 NPs showed further enhancement under NIR stimulation, with a 2.3-fold increase in ATE skin penetration. Furthermore, we verified in vivo that these JR400-MoS 2 NPs do not cause skin irritation suggesting that they are promising new TDDS candidates for small molecule drugs.

Objective: To investigate the effect of homocysteine (Hcy) on intestinal permeability in rats with TNBS/ethanol-induced colitis and elucidate its mechanism.Methods: Sprague-Dawley rats were divided into four groups: normal, normal + Hcy injection, TNBS model, and TNBS model + Hcy injection. Experimental colitis was induced by trinitrobenzene sulfonic acid (TNBS) in 50% ethanol; rats were injected subcutaneously with Hcy from the first day after the induction of experimental colitis on 30 consecutive days. To determine the severity of colitis, the disease activity index (DAI) was evaluated; colon tissues were collected for the detection of the activity of myeloperoxidase (MPO) and the contents of MDA, IL-1β, IL-6, TNF-α, MMP-2, and MMP-9. Intestinal epithelial permeability was assessed with Evans blue (EB) dye. The levels of Hcy in plasma and colon mucosa were measured by high-performance liquid chromatography-fluorescence detection (HPLC-FD).Results: Compared with the normal group, the DAI scoring and MPO activity, contents of MDA, IL-1β, IL-6, TNF-α, MMP-2, MMP-9 in the colon and EB in the small intestine were significantly increased in the TNBS group (P < 0.01). Compared with the TNBS model group, the DAI scoring, plasma and colonic mucosa Hcy levels, MPO activity and contents of MDA, IL-1β, IL-6, TNF-α, MMP-2, MMP-9 in colon and EB in small intestine were significantly increased in the TNBS-induced colitis rats with simultaneous Hcy injection (P < 0.01).Conclusion: Hcy can increase intestinal permeability and aggravate inflammatory damage in rats with TNBS-induced colitis, the underlying mechanisms of which may be attributed to its effects of promoting the expression of MMP-2 and MMP-9, leading to injury of the intestinal barrier.

Aim: This study investigated the effect of intragastrically administered melatonin on intestinal mucosal permeability induced by diclofenac in mice. Methods: Intestinal mucosal permeability was induced in mice by intragastric administration of diclofenac (2.5 mg/kg). Melatonin was given intragastrically (10 mg/kg) once per day for 3 d after diclofenac administration. The small intestine was examined macroscopically and microscopically for pathologic injury to the intestinal mucosa. Intestinal mucosal permeability was evaluated by Evans blue and FITC-dextran methods. Mitochondrial functional parameters, including mitochondrial membrane potential, mitochondrial ATPase and succinate dehydrogenase (SDH) activity, were assessed. The malondialdehyde (MDA) and myeloperoxidase (MPO) levels were determined from small intestinal mucosal homogenates. Results: As compared with control mice, the permeability, pathologic score, MDA and MPO levels and ulceration of the intestinal mucosa were increased significantly by diclofenac treatment, and a broadened junctional complex and enlarged intercellular space were observed by transmission electron microscopy (TEM). Melatonin treatment significantly reduced the intestinal mucosal permeability, pathologic score, MDA, and MPO levels and ulceration of the intestinal mucosa. By TEM, the small intestine villus morphology and intercellular spaces were nearly normal in melatonin-treated mice. At the level of the mitochondria, melatonin treatment significantly restored the activities of ATPase and SDH. Conclusion: The intestinal damage and increased intestinal permeability induced by diclofenac in mice was limited by melatonin; moreover, melatonin preserved several aspects of mitochondrial function.

Increased intestinal permeability induced by diclofenac can be attenuated by rebamipide, which partially contributed to the protection of mitochondrial function.

MYO9B gene polymorphisms may influence the sub-phenotypic expression of CD in China. No association between these MYO9B polymorphisms and intestinal permeability in IBD patients was found.