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The virtual try-on task is so attractive that it has drawn considerable attention in the field of computer vision. However, presenting the 3-D physical characteristic (e.g., pleat and shadow) based on a 2-D image is very challenging. Although there have been several previous studies on 2-D-based virtual try-on work, most: 1) required user-specified target poses that are not user-friendly and may not be the best for the target clothing and 2) failed to address some problematic cases, including facial details, clothing wrinkles, and body occlusions. To address these two challenges, in this article, we propose an innovative template-free try-on image synthesis (TF-TIS) network. The TF-TIS first synthesizes the target pose according to the user-specified in-shop clothing. Afterward, given an in-shop clothing image, a user image, and a synthesized pose, we propose a novel model for synthesizing a human try-on image with the target clothing in the best fitting pose. The qualitative and quantitative experiments both indicate that the proposed TF-TIS outperforms the state-of-the-art methods, especially for difficult cases.

To evaluate the long-term safety and effectiveness of tocilizumab (TCZ) for the treatment of rheumatoid arthritis (RA) in a real-world clinical setting in Taiwan.

Increasing evidence indicates a pathogenic role of deregulated autophagy in rheumatoid arthritis (RA). We examined the relationship between autophagy and inflammatory parameters in patients with RA receiving biologic therapy. In 72 patients with RA and 20 healthy control subjects (HC), autophagosome levels were determined by the mean fluorescence intensity (MFI) of autophagosomotropic dye incorporated into circulating immune cells, and p62 expression levels in immune cells were measured by flow cytometry. We used immunoblotting to examine protein expression of LC3-II and p62 in peripheral blood mononuclear cells. Patients with RA had significantly higher levels of autophagosome reflected by MFI of Cyto-ID in circulating lymphocytes, monocytes, and granulocytes (median values, 3.6, 11.6, and 64.8, respectively) compared with HC (1.9, 6.0, and 35.8; respectively) (all p< 0.001). p62 MFI levels in lymphocytes and granulocytes from patients with RA (17.1 and 8.6, respectively) were significantly lower than those in the corresponding cells from HC (20.2, p< 0.05; and 13.1, p< 0.001, respectively). Significantly higher levels of LC3-II protein expression in contrast to lower p62 protein levels were observed in patients with RA than in HC. The autophagosome levels in immune cells were significantly correlated with inflammatory parameters in patients with RA, and they were significantly decreased with disease remission after treatment with tumor necrosis factor-α inhibitors or interleukin-6 receptor inhibitor. Elevated autophagy with significant correlation to inflammation suggests the involvement of autophagy in RA pathogenesis. The effectiveness of biologic therapy might be partly related to the downregulation of autophagy expression.

Objective.The dysregulation of the NLRP3 (NLR containing a pyrin domain) inflammasome is involved in autoinflammatory diseases. Adult-onset Still disease (AOSD) is regarded as an autoinflammatory disease. However, the pathogenic involvement of NLRP3 inflammasome in AOSD remains unclear and NLRP3 activators in AOSD are currently unknown.Methods.The mRNA expression of NLRP3 inflammasome signaling in peripheral blood mononuclear cells (PBMC) from 34 patients with AOSD and 14 healthy subjects was determined using quantitative-PCR (qPCR). The changes in mRNA and protein levels of NLRP3 inflammasome signaling in PBMC treated with the potential activator [imiquimod (IMQ)] or inhibitor of NLRP3 were evaluated using qPCR and immunoblotting, respectively. The supernatant levels of interleukin (IL)-1β and IL-18 were determined by ELISA.Results.Significantly higher mRNA levels of NLRP3 inflammasome signaling were observed in patients with AOSD compared with healthy controls. NLRP3 expressions were positively correlated with disease activity in patients with AOSD. IMQ (an effective Toll-like receptor 7 ligand; 10 µg/ml and 25 µg/ml) stimulation of PBMC from patients with AOSD induced dose-dependent increases of mRNA expression of NLRP3 (mean ± standard error of the mean, 2.06 ± 0.46 and 6.05 ± 1.84, respectively), caspase-1 (1.81 ± 0.23 and 4.25 ± 0.48), IL-1β (5.68 ± 1.51 and 12.13 ± 3.71), and IL-18 (2.32 ± 0.37 and 4.81 ± 0.51) compared with controls (all p < 0.005). IMQ stimulation of PBMC from patients similarly induced greater increases in protein expressions of NLRP3 inflammasome compared with controls. The protein expressions of NLRP3, IL-1β, and IL-18 on PBMC significantly decreased after treatment with NLRP3 inhibitor in patients with AOSD.Conclusion.Increased expression of NLRP3 inflammasome and its positive correlation with disease activity in AOSD suggest its involvement in disease pathogenesis. IMQ upregulated expressions of NLRP3 inflammasome signaling, and IMQ might be an activator of NLRP3 inflammasome in AOSD.

Suicide is a global health issue, and an increase in suicide risk has been found in patients with systemic lupus erythematosus (SLE) when compared with the general population. However, only a few studies have described suicide attempts in patients with SLE in detail.

This article presents a convenient means to inter-relate appliances in an intelligent living space. While more and more wireless devices are phased in, a user can barely familiarize herself with managing these devices. This is because wireless devices often operate in some form of binding relationships among themselves, which are typically set up at startup in a self-organizing fashion, leaving the user little room for intervention. As a remedy, we propose a software-hardware codesign and implementation that enable the user to adapt network operations to certain needs anytime without knowledge of low-level details. Binding manipulation is done straightaway with simple mouse clicking and dragging on icons in our graphical user interface. We demonstrate example applications in green power systems as well. A practical platform over which to inspire other applications, this study elegantly lends itself to generic wireless network environments.

To investigate the association of body cell mass loss with disease activity and disability in rheumatoid arthritis patients.

OBJECTIVE: Interleukin 18 (IL-18) has a central role in the pathogenesis of adult-onset Still’s disease (AOSD). We investigated the functional association of –607 (C/A) IL-18 promoter polymorphisms with disease course in Chinese patients with AOSD. METHODS: Sequence-specific primer polymerase chain reaction and the restriction fragment-length polymorphism method were used to analyze the genotypes of IL-18 promoter polymorphism at position –607 in 96 unrelated patients with AOSD and 164 ethnically-matched healthy controls. Serum IL-18 levels were determined using ELISA in patients with active untreated AOSD. RESULTS: Significantly lower frequencies of single-nucleotide polymorphism –607/AA were observed in patients with AOSD compared to healthy controls (18.8% vs 31.1%, respectively; p < 0.05). Median levels of serum IL-18 were significantly lower in AOSD patients with AA genotype compared to those with CA genotype or CC genotype (147.5 pg/ml vs 410.5 pg/ml or 262.4 pg/ml, respectively; both p < 0.05). Significantly lower IL-18 levels were demonstrated in AOSD patients with a monocyclic systemic course than in those with a polycyclic systemic course or a chronic articular course. The AA genotype was more frequently observed in patients with monocyclic systemic course, which had the best prognosis, than in those with the other 2 disease courses. In contrast, a lower frequency of the AA genotype than the CA or the CC genotype was observed in patients with chronic disabling arthritis (5.5% vs 25.0% or 19.2%, respectively). CONCLUSION: The SNP –607/AA genotype with lower IL-18 levels might be a genetically protective factor for the occurrence of AOSD in the Chinese population, against progression of chronic disabling arthritis.

To determine spontaneous and activation‐induced apoptosis of peripheral blood lymphocytes (PBLs) from patients with active untreated adult‐onset Still's disease (AOSD) and to examine the role of interleukin‐18 (IL‐18) involved in the apoptosis related to this disease.The percentages of spontaneous and IL‐18–stimulated apoptotic lymphocytes in peripheral blood of 20 patients with active untreated AOSD, 20 with active untreated systemic lupus erythematosus (SLE), and 20 healthy controls were determined using annexin V/propidium iodide staining and flow cytometry. Serum IL‐18 levels were measured using enzyme‐linked immunosorbent assay. The transcripts of caspase 3 gene and apoptosis‐regulating genes, including Fas, FasL, Bcl‐2, and p53 in IL‐18–treated peripheral blood mononuclear cells (PBMCs) from 8 AOSD patients, 4 SLE patients, and 4 healthy controls, were examined by real‐time quantitative polymerase chain reaction.Significantly higher percentages of spontaneous and IL‐18–stimulated apoptotic PBLs were found in patients with active untreated AOSD and those with active untreated SLE than in healthy controls. The percentages of spontaneous and IL‐18–stimulated apoptotic lymphocytes correlated positively with clinical activity scores and serum IL‐18 levels for AOSD patients and SLE patients. The percentages of spontaneous and activation‐induced apoptotic PBLs significantly declined, paralleling clinical remission and the decrease in serum IL‐18 levels after effective therapy in AOSD patients. Up‐regulation of FasL and p53 transcripts was demonstrated in IL‐18–treated PBMCs from AOSD patients and SLE patients in a dose‐dependent manner.The increased apoptosis of PBLs from AOSD patients may be associated with the effect of IL‐18 through up‐regulation of FasL and p53 transcripts.

The objective of this study was to investigate the potential role of the Toll-like receptor 7 (TLR7) signaling pathway in the pathogenesis of adult-onset Still's disease (AOSD).

The objective of this study was to investigate the effects of tumor necrosis factor (TNF)-α inhibitors on circulating T helper-type 17 (Th17) cells and Th17-related cytokines in patients with rheumatoid arthritis (RA).