Journal of rheumatic diseases and treatment最新文献

{"title":"Multifocal Avascular Necrosis of the Lunate and Triquetrum in a Child with Systemic Lupus Erythematosus","authors":"D. Roberts, A. Jester, T. Southwood, K. Johnson, K. Oestreich","doi":"10.23937/2469-5726/1510063","DOIUrl":"https://doi.org/10.23937/2469-5726/1510063","url":null,"abstract":"Avascular necrosis is a known complication of systemic lupus erythematosus. We report an unusual case of avascular necrosis affecting both the lunate and triquetrum in a child with this condition. Vasculitis, synovitis and IgM anticardiolipin antibodies were probable predisposing factors. The use of arthroscopic synovial debridement improves symptoms even in the presence of carpal chondromalacia and potentially delays the need for salvage surgery. *Corresponding author: Darren Roberts, Department of Hand, Plastic and Reconstructive Surgery, Birmingham Children’s Hospital, UK, E-mail: robertsdc@doctors.org.uk CASe RepORT","PeriodicalId":73938,"journal":{"name":"Journal of rheumatic diseases and treatment","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85254664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Application of Behavioral Assays Allows Dissociation of Joint Pathology from Systemic Extra-Articular Alterations Induced by Inflammatory Arthritis.","authors":"Ann K Harvey, Mariah J Lelos, Claire J Greenhill, Ashley T Jones, Susanne P Clinch, Michael J Newton, Stephen B Dunnett, Sean L Wyatt, Anwen S Williams, Simon A Jones","doi":"10.23937/2469-5726/1510033","DOIUrl":"10.23937/2469-5726/1510033","url":null,"abstract":"<p><strong>Introduction: </strong>Although rheumatoid arthritis (RA) is a disease of articular joints, patients often suffer from co-morbid neuropsychiatric changes, such as anxiety, that may reflect links between heightened systemic inflammation and abnormal regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Here, we apply behavioral neuroscience methods to assess the impact of antigen-induced arthritis (AIA) on behavioral performance in wild type (WT) and interleukin-10 deficient (<i>Il10</i>^-/-) mice. Our aim was to identify limb-specific motor impairments, as well as neuropsychological responses to inflammatory arthritis.</p><p><strong>Methods: </strong>Behavioral testing was performed longitudinally in WT and <i>Il10</i>^-/- mice before and after the induction of arthritic joint pathology. Footprint analysis, beam walking and open field assessment determined a range of motor, exploratory and anxiety-related parameters. Specific gene changes in HPA axis tissues were analyzed using qPCR.</p><p><strong>Results: </strong>Behavioral assessment revealed transient motor and exploratory impairments in mice receiving AIA, coinciding with joint swelling. Hind limb coordination deficits were independent of joint pathology. Behavioral impairments returned to baseline by 10 days post-AIA in WT mice. <i>Il10</i>^-/- mice demonstrated comparable levels of swelling and joint pathology as WT mice up to 15 days post-AIA, but systemic differences were evident in mRNA expression in HPA axis tissues from <i>Il10</i>^-/- mice post-AIA. Interestingly, the behavioral profile of <i>Il10</i>^-/- mice revealed a significantly longer time post-AIA for activity and anxiety-related behaviors to recover.</p><p><strong>Conclusions: </strong>The novel application of sensitive behavioral tasks has enabled dissociation between behaviors that occur due to transient joint-specific pathology and those generated by more subtle systemic alterations that manifest post-AIA.</p>","PeriodicalId":73938,"journal":{"name":"Journal of rheumatic diseases and treatment","volume":"2 2","pages":"1510033"},"PeriodicalIF":0.0,"publicationDate":"2016-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7614560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9896431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of experimental arthritis through AMP-activated protein kinase activation and autophagy modulation.","authors":"Huimin Yan,&nbsp;Hui-Fang Zhou,&nbsp;Ying Hu,&nbsp;Christine T N Pham","doi":"10.23937/2469-5726/1510005","DOIUrl":"https://doi.org/10.23937/2469-5726/1510005","url":null,"abstract":"<p><p>Autophagy plays a central role in various disease processes. However, its contribution to inflammatory arthritides such as rheumatoid arthritis (RA) is unclear. We observed that autophagy is engaged in the K/BxN serum transfer model of RA but autophagic flux is severely impaired. Metformin is an anti-diabetic drug that has been shown to stimulate autophagy. Induction of autophagic flux, through metformin-mediated AMP-activated protein kinase (AMPK) activation and interruption of mammalian target of rapamycin (mTOR) signaling mitigated the inflammation in experimental arthritis. Further investigation into the effects of metformin suggest that the drug directly activates AMPK and dose-dependently suppressed the release of TNF-α, IL-6, and MCP-1 by macrophages while enhancing the release of IL-10 <i>in vitro. In vivo</i>, metformin treatment significantly suppressed clinical arthritis and inflammatory cytokine production. Mechanistic studies suggest that metformin exerts its anti-inflammatory effects by correcting the impaired autophagic flux observed in the K/BxN arthritis model and suppressing NF-κB-mediated signaling through selective degradation of IκB kinase (IKK). These findings establish a central role for autophagy in inflammatory arthritis and argue that autophagy modulators such as metformin may represent potential therapeutic agents for the treatment of RA.</p>","PeriodicalId":73938,"journal":{"name":"Journal of rheumatic diseases and treatment","volume":"1 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2015-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479345/pdf/nihms670734.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33303083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aspirin-Triggered Resolvin D1 Versus Dexamethasone in the Treatment of Sjögren's Syndrome-Like NOD/ShiLtJ Mice - A Pilot Study.","authors":"Justin T Easley,&nbsp;Joel W Nelson,&nbsp;Rachel E Mellas,&nbsp;Salah Sommakia,&nbsp;Chunhua Wu,&nbsp;Bryan Trump,&nbsp;Olga J Baker","doi":"10.23937/2469-5726/1510027","DOIUrl":"https://doi.org/10.23937/2469-5726/1510027","url":null,"abstract":"<p><p>Resolvin D1 (RvD1) and its aspirin-triggered epimeric form (AT-RvD1) are endogenous lipid mediators (derived from docosahexaenoic acid, DHA) that control the duration and magnitude of inflammation in models of complex diseases. Our previous studies demonstrated that RvD1-mediated signaling pathways are expressed and active in salivary glands from rodents and humans. Furthermore, treatment of salivary cells with RvD1 blocked TNF-α-mediated inflammatory signals and improved epithelial integrity. The purpose of this pilot study was to determine the feasibility of treatment with AT-RvD1 versus dexamethasone (DEX) on inflammation (i.e., lymphocytic infiltration, cytokine expression and apoptosis) observed in submandibular glands (SMG) from the NOD/ShiLtJ Sjögren's syndrome (SS) mouse model before experimenting with a larger population. NOD/ShiLtJ mice were treated intravenously with NaCl (0.9%, negative control), AT-RvD1 (0.01-0.1 mg/kg) or DEX (4.125-8.25 mg/kg) twice a week for 14 weeks beginning at 4 weeks of age. At 18 weeks of age, SMG were collected for pathological analysis and detection of SS-associated inflammatory genes. The AT-RvD1 treatment alone did not affect lymphocytic infiltration seen in NOD/ShiLtJ mice while DEX partially prevented lymphocytic infiltration. Interestingly, both AT-RvD1 and DEX caused downregulation of SS-associated inflammatory genes and reduction of apoptosis. Results from this pilot study suggest that a systemic treatment with AT-RvD1 and DEX alone attenuated inflammatory responses observed in the NOD/ShiLtJ mice; therefore, they may be considered as potential therapeutic tools in treating SS patients when used alone or in combination.</p>","PeriodicalId":73938,"journal":{"name":"Journal of rheumatic diseases and treatment","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841619/pdf/nihms759962.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34488050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of Burnout among Physicians at King Salman Armed Forces Hospital, Tabuk, Saudi Arabia","authors":"Nora Mohamed, Mohammad Sidiq, H. Alblewi, Mehul Contractor","doi":"10.33805/2694-2216.107","DOIUrl":"https://doi.org/10.33805/2694-2216.107","url":null,"abstract":"Introduction: Physician burnout in armed forces involves emotional exhaustion, depersonalization and a sense of declined personal accomplishment. This can have an adverse effect on quality patient care, the healthcare team and can cost physician health in both in-training physicians and practicing physicians. The causative factors include excessive long work shifts, inefficient work systems and clerical burdens, professional home conflicts, lack of departmental support, limited work force and poor leadership culture. Objectives: This study aims at measuring the prevalence of burnout in physicians working in King Salman armed forces hospital Saudi Arabia and studying possible related socio-demographic variables. Methods: A cross sectional study was conducted between April and May 2015 among physicians. A self‑administered questionnaire was used that includes questions on socio demographic characteristics, sources of stress and burnout of the Maslach Burnout Inventory-Human Services Survey (MBI-HSS) in this study. Student’s T-test and chi square tests were used for analysis. Results: Majority were males 74.8% aged more than 35 years with the prevalence rate of 14.2%. The analyzed variables associated with emotional exhaustion, the following factors significantly affected the EE with P value<0.05, exercise, alternate shift duty, work over load, quality of life, satisfaction with work and specialty. As for the significant factors associated with DP, shift duty, work overload, quality of life perception and specialty were found to have P value less than 0.05. Conclusion: Burnout is prevalent among physicians; we identified variables significantly associated with Emotional exhaustion (EE), Depersonalization (DP) and Personal accomplishment (PA). However, further research is recommended to study other predictors not mentioned in the current study and all health policy makers must work jointly in designing and implement effective remedial measures for physician burnout.","PeriodicalId":73938,"journal":{"name":"Journal of rheumatic diseases and treatment","volume":"79 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84109879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}