Effects of HSP60 and LPS on HO-1 protein expression in PBMCs from patients with BD

Effect of lipopolysaccharide (LPS) stimulation on heme oxygenase (HO)-1 and actin protein expression in peripheral blood mononuclear cells (PBMCs) from patients with Behçet's disease (BD). PBMCs from a BD patient were stimulated with LPS in the presence or absence of 10 ng/ml interleukin (IL)-10 and 100 μg/ml polymyxin B (PMB). Representative immunoblotting data for HO-1 protein in the cells are shown. The arrowhead indicates 32 kDa molecular weight HO-1 specific band. Effect of heat shock protein (HSP)60 (3 μg/ml) stimulation on endogenous HO-1 protein expression in PBMCs from patients with BD. The arrowhead indicates 32 kDa HO-1 specific band. A representative of three independent experiments is shown. Mean and standard error of the mean (SEM) values of HO-1 and actin protein expression in PBMCs stimulated by LPS (1 ng/ml) for 24 hours in patients with BD (= 14). < 0.001, as determined using paired -test. Effect of infliximab (10 μg/ml) or IgGκ (10 μg/ml) on HO-1 expression in LPS (10 ng/ml) or tumor necrosis factor (TNF; 1 ng/ml) treated PBMCs.<p><b>Copyright information:</b></p><p>Taken from "Association of reduced heme oxygenase-1 with excessive Toll-like receptor 4 expression in peripheral blood mononuclear cells in Behçet's disease"</p><p>http://arthritis-research.com/content/10/1/R16</p><p>Arthritis Research & Therapy 2008;10(1):R16-R16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2374472.</p><p></p

Effect of forced HO-1 expression on Toll-like receptor (TLR)2 and TLR4 mRNA expression in peripheral monocytes

Immunoblotting analysis of heme oxygenase (HO)-1 and actin in pHO-1 (human HO-1 expression vector) or pCont (control vector) transfected monocytes. The arrow represents HO-1 protein. Real-time PCR analysis of TLR2 and TLR4 mRNA expression in pHO-1 transfected peripheral blood mononuclear cells (PBMCs). NS, not significant.<p><b>Copyright information:</b></p><p>Taken from "Association of reduced heme oxygenase-1 with excessive Toll-like receptor 4 expression in peripheral blood mononuclear cells in Behçet's disease"</p><p>http://arthritis-research.com/content/10/1/R16</p><p>Arthritis Research & Therapy 2008;10(1):R16-R16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2374472.</p><p></p

On-demand ultrasonography assessment in the most symptomatic joint supports the 8-joint score system for management of rheumatoid arthritis patients

<p><i>Objectives</i>: To investigate whether on-demand ultrasonography (US) assessment alongside a routine examination is useful in the management of rheumatoid arthritis (RA).</p> <p><i>Methods</i>: US was performed in eight (bilateral MCP 2, 3, wrist and knee) joints as the routine in a cumulative total of 406 RA patients. The most symptomatic joint other than the routine joints was additionally scanned. Power Doppler (PD) and gray-scale images were scored semiquantitatively. Eight-joint scores were calculated as the sum of individual scores for the routine joints.</p> <p><i>Results</i>: The most symptomatic joint was found among the routine joints in 209 patients (Group A) and in other joints in 148 (Group B). The PD scores of the most symptomatic joint correlated well with the 8-joint scores in Group A (r_s = 0.66), but not in Group B (r_s = 0.33). The sensitivity and specificity of assessment of the most symptomatic joint for routine assessment positivity were high (84.0% and 100%, respectively) in Group A, but low (50.0% and 61.8%, respectively) in Group B. Additional examination detected synovitis in 38% of Group B with negative results in the routine.</p> <p><i>Conclusions</i>: On-demand US assessment in the most symptomatic joint, combined with the routine assessment, is useful for detecting RA synovitis.</p

¹⁸F-FDG and ¹⁸F-NaF PET/CT demonstrate coupling of inflammation and accelerated bone turnover in rheumatoid arthritis

<p><i>Objective.</i> To compare the findings in rheumatoid arthritis (RA)-affected joints between ¹⁸F-fluorodeoxyglucose (FDG) and ¹⁸F-fluoride (NaF) positron emission tomography (PET)/computed tomography (CT).</p> <p><i>Methods.</i> We enrolled twelve RA patients who started a new biologic agent (naïve 9 and switch 3). At entry, both hands were examined by ¹⁸F-FDG PET/CT, ¹⁸F-NaF PET/CT, and X-ray. Intensity of PET signals was determined by standardized uptake value max (SUVmax) in metacarpophalangeal (MCP), proximal interphalangeal (PIP), and ulnar, medial, and radial regions of the wrists. Hand X-rays were evaluated according to the Genant-modified Sharp score at baseline and 6 months.</p> <p><i>Results.</i> Both ¹⁸F-FDG and ¹⁸F-NaF accumulated in RA-affected joints. The SUVmax of ¹⁸F-FDG correlated with that of ¹⁸F-NaF in individual joints (<i>r</i> = 0.65), though detail distribution was different between two tracers. ¹⁸F-NaF and ¹⁸F-FDG signals were mainly located in the bone and the surrounding soft tissues, respectively. The sum of SUVmax of ¹⁸F-NaF correlated with disease activity score in 28 joint (DAS28), modified health assessment questionnaire (MHAQ), and radiographic progression. ¹⁸F-FDG and ¹⁸F-NaF signals were associated with the presence of erosions, particularly progressive ones.</p> <p><i>Conclusion.</i> Our data show that both ¹⁸F-FDG and ¹⁸F-NaF PET signals were associated with RA-affected joints, especially those with ongoing erosive changes.</p

Consensus-based identification of factors related to false-positives in ultrasound scanning of synovitis and tenosynovitis

<div><p></p><p>Introduction</p><p>We aimed to identify causes of false-positives in ultrasound scanning of synovial/tenosynovial/bursal inflammation and provide corresponding imaging examples.</p><p>Methods</p><p>We first performed systematic literature review to identify previously reported causes of false-positives. We next determined causes of false-positives and corresponding example images for educational material through Delphi exercises and discussion by 15 experts who were an instructor and/or a lecturer in the 2013 advanced course for musculoskeletal ultrasound organized by Japan College of Rheumatology Committee for the Standardization of Musculoskeletal Ultrasonography (JCR-CoSMUS).</p><p>Results</p><p>Systematic literature review identified 11 articles relevant to sonographic false-positives of synovial/tenosynovial inflammation. Based on these studies, 21 candidate causes of false-positives were identified in the consensus meeting. Of these items, 11 achieved a pre-defined consensus (≥ 80 %) in Delphi exercise and were classified as follows: I. Gray-scale assessment (A. Non-specific synovial findings, B. Normal anatomical structures which can mimic synovial lesions due to either their low echogenicity or anisotropy); II. Doppler assessment (A. Intra-articular normal vessels, B. Reverberation). Twenty-four corresponding examples with 49 still and 23 video images also achieved consensus.</p><p>Conclusions</p><p>Our study provides a set of representative images that can help sonographers to understand false-positives in ultrasound scanning of synovitis and tenosynovitis.</p></div

Additional file 2: Table S2. of Continuous evolution of clinical phenotype in 578 Japanese patients with Behçet’s disease: a retrospective observational study

Phenotype of patients with BD treated with biologic agents. (DOC 29 kb

Additional file 3: Table S3. of Continuous evolution of clinical phenotype in 578 Japanese patients with Behçet’s disease: a retrospective observational study

Rate of therapeutic agents use in groups with different date of onset. (DOC 31 kb

Additional file 1 of Evaluating the safety profile of calcineurin inhibitors: cancer risk in patients with systemic lupus erythematosus from the LUNA registry—a historical cohort study

Additional file 1: Figure S1. Design diagram to clarify the key points of each item

Additional file 2: Table S2. of The predictive prognostic factors for polymyositis/dermatomyositis-associated interstitial lung disease

Comparison of demographic data among each PM/DM subtype in PM/DM-ILD patients. (PDF 102 kb

Association of Functional Polymorphisms in <i>Interferon Regulatory Factor 2</i> (<i>IRF2</i>) with Susceptibility to Systemic Lupus Erythematosus: A Case-Control Association Study

<div><p>Interferon regulatory factor 2 (IRF2) negatively regulates type I interferon (IFN) responses, while it plays a role in induction of Th1 differentiation. Previous linkage and association studies in European-American populations suggested genetic role of <i>IRF2</i> in systemic lupus erythematosus (SLE); however, this observation has not yet been confirmed. No studies have been reported in the Asian populations. Here we investigated whether <i>IRF2</i> polymorphisms contribute to susceptibility to SLE in a Japanese population. Association study of 46 <i>IRF2</i> tag single nucleotide polymorphisms (SNPs) detected association of an intronic SNP, rs13146124, with SLE. When the association was analyzed in 834 Japanese patients with SLE and 817 healthy controls, rs13146124 T was significantly increased in SLE compared with healthy controls (dominant model, P = 5.4×10⁻⁴, Bonferroni-corrected P [Pc] = 0.026, odds ratio [OR] 1.48, 95% confidence interval [CI] 1.18–1.85). To find causal SNPs, resequencing was performed by next-generation sequencing. Twelve polymorphisms in linkage disequilibrium with rs13146124 (r²: 0.30–1.00) were identified, among which significant association was observed for rs66801661 (allele model, P = 7.7×10⁻⁴, Pc = 0.037, OR 1.53, 95%CI 1.19–1.96) and rs62339994 (dominant model, P = 9.0×10⁻⁴, Pc = 0.043, OR 1.46, 95%CI 1.17–1.82). The haplotype carrying both of the risk alleles (rs66801661A–rs62339994A) was significantly increased in SLE (P = 9.9×10⁻⁴), while the haplotype constituted by both of the non-risk alleles (rs66801661G–rs62339994G) was decreased (P = 0.0020). A reporter assay was carried out to examine the effect of the <i>IRF2</i> haplotypes on the transcriptional activity, and association of the <i>IRF2</i> risk haplotype with higher transcriptional activity was detected in Jurkat T cells under IFNγ stimulation (Tukey's test, P = 1.2×10⁻⁴). In conclusion, our observations supported the association of <i>IRF2</i> with susceptibility to SLE, and the risk haplotype was suggested to be associated with transcriptional activation of <i>IRF2</i>.</p></div