Explore the vast range of titles available.

KIAA1199 has a strong hyaluronidase activity in inflammatory arthritis. This study aimed to identify a drug that could reduce KIAA1199 activity and clarify its effects on inflammatory arthritis. Rat chondrosarcoma (RCS) cells were strongly stained with Alcian blue (AB). Its stainability was reduced in RCS cells, which were over-expressed with the KIAA1199 gene (RCS-KIAA). We screened the drugs that restore the AB stainability in RCS-KIAA. The effects of the drug were evaluated by particle exclusion assay, HA ELISA, RT-PCR, and Western blotting. We further evaluated the HA accumulation and the MMP1 and three expressions in fibroblast-like synoviocytes (FLS). In vivo, the effects of the drug on symptoms and serum concentration of HA in a collagen-induced arthritis mouse were evaluated. Ipriflavone was identified to restore AB stainability at 23%. Extracellular matrix formation was significantly increased in a dose-dependent manner (p = 0.006). Ipriflavone increased the HA accumulation and suppressed the MMP1 and MMP3 expression on TNF-α stimulated FLS. In vivo, Ipriflavone significantly improved the symptoms and reduced the serum concentrations of HA. Conclusions: We identified Ipriflavone, which has inhibitory effects on KIAA1199 activity. Ipriflavone may be a therapeutic candidate based on its reduction of KIAA1199 activity in inflammatory arthritis.

To evaluate Safety and efficacy of probiotic supplementation in inflammatory arthritis. The literature on the treatment of inflammatory arthritis with probiotics has been collected in databases such as CNKI, Pubmed, Cochrane library, Embase, etc. The search time is for them to build the database until May 2022. The included literatures are randomized controlled trials (RCTs) of probiotics in the treatment of hyperuricemia and gout. The Cochrane risk assessment tool was used for quality evaluation, and the Rev Man5.3 software was used for meta-analysis. A total of 37 records were finally included, involving 34 RCTs and 8 types of autoimmune disease (Hyperuricemia and gout, Inflammatory bowel disease arthritis, juvenile idiopathic arthritis [JIA], Osteoarthritis [OA], Osteoporosis and Osteopenia, Psoriasis, rheumatoid arthritis (RA), Spondyloarthritis). RA involved 10 RCTs (632 participants) whose results showed that probiotic intervention reduced CRP. Psoriasis involved 4 RCTs (214 participants) whose results showed that probiotic intervention could reduce PASI scores. Spondyloarthritis involved 2 RCTs (197 participants) whose results showed that probiotic intervention improved symptoms in patients. Osteoporosis and Ostepenia involving 10 RCTs (1156 participants) showed that probiotic intervention improved bone mineral density in patients. Hyperuricemia and gout involving 4 RCTs (294 participants) showed that probiotic intervention improved serum uric acid in patients. OA involving 1 RCTs (433 participants) showed that probiotic intervention improved symptoms in patients. JIA involving 2 RCTs (72 participants) showed that probiotic intervention improved symptoms in patients. Inflammatory bowel disease arthritis involving 1 RCTs (120 participants) showed that probiotic intervention improved symptoms in patients. All of the above RCTs showed that probiotics did not increase the incidence of adverse events. Probiotic supplements may improve Hyperuricemia and gout, Inflammatory bowel disease arthritis, JIA, OA, Osteoporosis and Osteopenia, Psoriasis, RA, Spondyloarthritis. However, more randomized controlled trials are needed in the future to determine the efficacy and optimal dosing design of probiotics. https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021286425, identifier CRD42021286425.

Abstract In the last decade, studies into sedentary behaviour in inflammatory arthritis have raised important questions regarding its role in this condition. Specifically, evidence is needed on whether sedentary behaviour might exacerbate adverse inflammatory arthritis outcomes, and whether reducing sedentary behaviour might offer an effective avenue for self-management in this population. Research exploring these important research questions is still very much in its infancy and lacks the direction and scientific rigour required to inform effective intervention design, delivery and evaluation. Behavioural epidemiology refers to research that aims explicitly to understand and influence health behaviour patterns to prevent disease and improve health. To this end, the Behavioural Epidemiology Framework specifies a focused approach to health behaviour research, which leads to the development of evidence-based interventions directed at specific populations. In this review, we introduce the Behavioural Epidemiology Framework in the context of research into sedentary behaviour in inflammatory arthritis and ask: where are we, and where do we need to go? Lay Summary What does this mean for patients? In the last few years, an increasing amount of research has started to investigate the links between sedentary behaviour, or sitting time, and health among people living with inflammatory arthritis. Overall, this research provides an initial indication that people living with inflammatory arthritis who spend more time sitting (and expending little energy) might experience worse outcomes, such as increased pain, fatigue and poorer physical function. However, there is still very little research being carried out in this area, and the research that has been done to date is very varied with regard to the scientific approach taken and the outcomes that have been studied. A more focused and systematic approach to research in this area is needed, so that researchers approach questions regarding the role of sitting time in inflammatory arthritis in the same way. In this way, we can generate a larger body of scientific evidence that can be used to design new ways, or interventions, that are more likely to help people living with inflammatory arthritis to reduce their sitting time and improve their health. In this article, we introduce a systematic approach to research that can be applied to understand how sitting time might be related to inflammatory arthritis-specific outcomes and overall health, in order to design these interventions. In introducing this approach, we highlight studies into sitting time in inflammatory arthritis that have already been conducted, and outline the research that we propose needs to be done to move this scientific field forward.

Abstract Regular physical activity is important for both physical and mental health. This is particularly important for people with inflammatory arthritis, because of the benefits on both disease-specific and systemic outcomes and the increased risk of comorbidities such as cardiovascular disease. Despite a wealth of evidence supporting physical activity interventions, there remains a significant gap in implementation into routine care. This overview describes what implementation is, examines why it is important to consider implementation approaches to improve uptake of physical activity, highlights factors that influence successful implementation using exemplars from both osteoarthritis and inflammatory arthritis and recommends where future research is needed. Lay Summary Regular physical activity is important for physical and mental health in people with arthritis. Physical activity may help arthritis symptoms and reduce the chances of developing other conditions such as heart disease. However, physical activity is not routinely recommended to all. Physical activity programs are not offered to everyone with arthritis who may benefit. This is called an implementation gap. This overview describes what implementation is and how it can be used to improve physical activity uptake. We report examples of successful physical activity implementation for arthritis and recommend where more research is needed.

Objective：Contrast-enhanced ultrasound （CEUS） is a well-established imaging modality which has been put into clinical use in recent years with the development of second-generation contrast agent and imaging devices,and its applications in the assessment of inflammatory arthritis,such as rheumatoid arthritis,psoriatic arthritis,and ankylosing spondylitis,have provoked abundant discussion and researches among radiologists and rheumatologists.To summarize the achievements of clinical studies on CEUS in the application of arthritis,and to keep up with the latest progresses of the imaging technique,we reviewed the literature in recent years,hoping to establish the role of CEUS in joint diseases.Data Sources：PubMed and EMBASE.Study Selection：We searched the database with the conditions ＂contrast-enhanced ultrasound AND arthritis＂ with the time limitation of recent 10 years.Clinical studies applying CEUS in inflammatory arthritis and review articles about development of CEUS in joint diseases in English were selected.Results：As it is proved by most studies in recent years,by delineating microvasculature within the inflamed joints,CEUS can indicate early arthritis with high sensitivity and specificity.Moreover,the imaging of CEUS has been proved to be consistent with histopathological changes of inflammatory arthritis.Quantitative analysis of CEUS permits further evaluation of disease activity.CEUS also plays a significant role in the therapeutic monitoring of the disease,which has been backed up by a number of studies.Conclusions：CEUS may be a new choice for the rheumatologists to evaluate inflammatory arthritis,because of its low price,ability to provide dynamic pictures,and high sensitivity to angiogenesis.It can also be applied in disease classification and therapeutic monitoring.More studies about CEUS need to be done to set up the diagnostic standards.

ObjectiveTo evaluate the long-term safety profile for upadacitinib across rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS) and atopic dermatitis (AD).MethodsSafety data from clinical trials of upadacitinib 15 mg and upadacitinib 30 mg (AD only) for treating RA, PsA, AS and AD as of 30 June 2021 were analysed; some RA and PsA studies included adalimumab and methotrexate as active comparators. Treatment-emergent adverse events (TEAEs) were presented by disease as exposure-adjusted event rates per 100 patient years (E/100 PY).ResultsThe analysis included 6991 patients (RA, n=3209; PsA, n=907; AS, n=182; AD, n=2693) who received at least one dose of upadacitinib, representing 15 425 PY of exposure (maximum duration 2.75–5.45 years) across diseases. Rates (E/100 PY) of any TEAE (205.5–278.1) and TEAE leading to discontinuation (4.5–5.4) were similar across diseases; serious TEAEs were numerically higher in patients with RA and PsA. Rates of herpes zoster (1.6–3.6), non-melanoma skin cancer (0–0.8) and elevations in creatine phosphokinase levels (4.4–7.9) were higher with upadacitinib than with active comparators in the RA and PsA populations. Deaths (0–0.8), serious infections (0–3.9), major adverse cardiovascular events (0–0.4), venous thromboembolism (<0.1–0.4) and malignancies (0.3–1.4) were observed, with rates generally lowest in AS and AD. Increased rates of acne were observed in patients with AD only.ConclusionsFindings from this analysis demonstrate that upadacitinib is generally well tolerated with observed differences in safety profiles likely reflective of varying patient characteristics across RA, PsA, AS and AD populations.Trial registration numbersNCT02675426, NCT02706951, NCT02706847, NCT02629159, NCT02706873, NCT03086343, NCT03104374, NCT03104400, NCT03178487, NCT03569293, NCT03568318 and NCT03607422.

ObjectiveAssess cancer risks with Janus kinase inhibitors (JAKi) versus biological disease-modifying antirheumatic drugs (bDMARDs) in clinical practice.MethodsCohort study of patients with rheumatoid arthritis (RA) or psoriatic arthritis (PsA) initiating treatment with JAKi, tumour necrosis factor inhibitors (TNFi) or other (non-TNFi) bDMARDs 2016–2020 using prospectively collected data from the Swedish Rheumatology Quality Register linked to other registers including the Cancer Register. We estimated incidence rates, and HRs via Cox regression, for all cancers excluding non-melanoma skin cancer (NMSC), and for individual cancer types including NMSC.ResultsWe identified 10 447 patients with RA and 4443 patients with PsA who initiated treatment with JAKi, a non-TNFi bDMARD or a TNFi. Median follow-up times in RA were 1.95, 2.83 and 2.49 years, respectively. In RA, based on 38 incident cancers other than NMSC with JAKi vs 213 with TNFi the overall HR was 0.94 (95% CI 0.65 to 1.38). Based on 59 vs 189 incident NMSC, the HR was 1.39 (95% CI 1.01 to 1.91). At 2 or more years since treatment start, the HR for NMSC was 2.12 (95% CI 1.15 to 3.89). In PsA, based on 5 vs 73 incident cancers other than NMSC, and 8 vs 73 incident NMSC, the corresponding HRs were 1.9 (95% CI 0.7 to 5.2) and 2.1 (95% CI 0.8 to 5.3).ConclusionIn clinical practice, the short-term risk of cancer other than NMSC in individuals initiating treatment with JAKi is not higher than for TNFi, but we found evidence of increased risk for NMSC.

Interleukin (IL)-4 and IL-13 belong to the T helper 2 (Th2) cytokine family, along with IL-3, IL-5, and IL-9. These cytokines are key mediators of allergic inflammation. They have important immunomodulatory activities and exert influence on a wide variety of immune cells, such as B cells, eosinophils, basophils, monocytes, fibroblasts, endothelial cells, airway epithelial cells, smooth muscle cells, and keratinocytes. Recent studies have implicated IL-4 and IL-13 in the development of various autoimmune diseases. Additionally, these cytokines have emerged as potential players in pathogenesis of inflammatory arthritis. Recent findings suggest that the IL-4 and IL-13 might play a significant role in the downregulation of inflammatory processes underlying RA pathology, and beneficially modulate the course of the disease. This review summarizes the biological features of the IL-4 and IL-13 and provides current knowledge regarding the role of these cytokines in inflammatory arthritis.

ObjectivesTo investigate the effect of the L-arginine metabolism on arthritis and inflammation-mediated bone loss.MethodsL-arginine was applied to three arthritis models (collagen-induced arthritis, serum-induced arthritis and human TNF transgenic mice). Inflammation was assessed clinically and histologically, while bone changes were quantified by μCT and histomorphometry. In vitro, effects of L-arginine on osteoclast differentiation were analysed by RNA-seq and mass spectrometry (MS). Seahorse, Single Cell ENergetIc metabolism by profilIng Translation inHibition and transmission electron microscopy were used for detecting metabolic changes in osteoclasts. Moreover, arginine-associated metabolites were measured in the serum of rheumatoid arthritis (RA) and pre-RA patients.ResultsL-arginine inhibited arthritis and bone loss in all three models and directly blocked TNFα-induced murine and human osteoclastogenesis. RNA-seq and MS analyses indicated that L-arginine switched glycolysis to oxidative phosphorylation in inflammatory osteoclasts leading to increased ATP production, purine metabolism and elevated inosine and hypoxanthine levels. Adenosine deaminase inhibitors blocking inosine and hypoxanthine production abolished the inhibition of L-arginine on osteoclastogenesis in vitro and in vivo. Altered arginine levels were also found in RA and pre-RA patients.ConclusionOur study demonstrated that L-arginine ameliorates arthritis and bone erosion through metabolic reprogramming and perturbation of purine metabolism in osteoclasts.

ObjectivesTo determine whether clinical tenderness can be considered a sign of inflammatory joint activity in patients with rheumatoid arthritis (RA), osteoarthritis (OA) or psoriatic arthritis (PsA) and to assess other possible factors associated with tenderness.MethodsPatients diagnosed with RA, PsA and OA underwent clinical and ultrasound examination of wrists and finger joints. Radiographs of the hands were scored for erosions, joint space narrowing (JSN), osteophytes and malalignment. A binary damage score (positive if ≥1 erosion, JSN and/or presence of malalignment) was calculated. Differences in grey scale signs of synovitis and power Doppler (PD) between tender non-swollen (TNS) versus non-tender non-swollen (NTNS) joints were calculated. Disease duration was assessed,<2 years was regarded as early and >5 years as long-standing arthritis.ResultsIn total, 34 patients (9 early and 14 long-standing) from patients with RA, 31 patients (7 early and 15 long-standing) with PsA and 30 with OA were included. We found equal frequencies of PD signal between TNS and NTNS joints in RA (p=0.18), PsA (p=0.59) or OA (p=0.96). However, PD had a significant association with tenderness in early arthritis both in RA (p=0.02) and in PsA (p=0.02). The radiographic damage score showed significant association with tenderness in RA (p<0.01), PsA (p<0.01) and OA (p=0.04).ConclusionTenderness might not always be a sign of active inflammation in RA, PsA and OA. While tenderness in early arthritis may be more related to inflammation, established disease is better explained by joint damage and malalignment.