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Aim: A challenge to the medical care of patients with rheumatoid arthritis (RA) is the management of the wide variety of information, including medication history and disease status, obtained from multiple sources to inform treatment decisions. To address this important clinical issue, we developed a data management system, based on smart device technology, and evaluated the benefit of this information to medical experts in helping them to form an impression of patients' health and disease, and treatment status before examination. Methods: Fifty‐seven patients with RA input relevant information about their condition and responses to a self‐report health assessment questionnaire into a smart device template before their scheduled examination. The efficacy of the system was assessed as a decrease in examination time at each visit, and the correlation between the self‐reported Multi‐Dimensional Health Assessment Questionnaire and the 28‐joint Disease Activity Score 28‐joint count erythrocyte sedimentation rate (DAS28‐ESR), which was used as a gold standard. Results: Examination duration was reduced in most patients at each visit. During the study, there were no limitations for patients with poor eyesight or severe arthropathy in using the system. In fact, the majority of patients found the smart technology to be easier to use than hand‐written questionnaires and health forms, regardless of age and disease activity. Conclusions: Our findings support the use of smart technology to provide accurate patient‐specific data and to streamline the process of medical care for patients with RA. [ABSTRACT FROM AUTHOR]

We have previously shown that the inhibition of connective tissue growth factor (CTGF) is a potential therapeutic strategy against rheumatoid arthritis (RA). CTGF consists of four distinct modules, including the insulin-like growth factor binding protein (IGFBP). In serum, insulin-like growth factors (IGFs) bind IGFBPs, interact with the IGF-1 receptor (IGF-1 R), and regulate anabolic effects and bone metabolism. We investigated the correlation between IGF-1 and the pathogenesis of RA, and the inhibitory effect on osteoclastogenesis and angiogenesis of the small molecular weight kinase inhibitor of the IGF-1 R, NVP-AEW541, against pathogenesis of RAin vitro. Cell proliferation was evaluated by cell count and immunoblotting. The expression of IGF-1 and IGF-1 R was evaluated by RT-PCR. Osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase staining, a bone resorption assay, and osteoclast-specific enzyme production. Angiogenesis was evaluated by a tube formation assay using human umbilical vein endothelial cells (HUVECs). The proliferation of MH7A cells was found to be inhibited in the presence of NVP-AEW541, and the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt was downregulated in MH7A cells. IGF-1 and IGF-1 R mRNA expression levels were upregulated during formation of M-colony stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL)-mediated osteoclast formation. Moreover, osteoclastogenesis was suppressed in the presence of NVP-AEW541. The formation of the tubular network was enhanced by IGF-1, and this effect was neutralized by NVP-ARE541. Our findings suggest that NVP-AEW541 may be utilized as a potential therapeutic agent in the treatment of RA. [ABSTRACT FROM AUTHOR]

MicroRNA (miRNA) is small RNA of 20 to 22 nucleotides in length and is stably present in plasma. Regulating the expression of miRNA taken into cells has been suggested as a general therapeutic approach. We identified the novel anti-inflammatory miRNA hsa-miR-766-3p and investigated its biological function in human rheumatoid arthritis (RA) fibroblast-like synoviocyte MH7A cells. To verify the function of the miRNA present in the plasma of RA patients, we performed a comprehensive analysis of the miRNA expression during abatacept treatment and identified eight miRNAs with significantly altered expression levels. Among these eight miRNAs, miR-766-3p was found to have a clear function. The expression of inflammatory genes in response to inflammatory stimuli was suppressed in MH7A transduced with miR-766-3p. We showed that miR-766-3p indirectly reduced the activation of NF-κB and clarified that this mechanism was partially involved in the reduction of the mineralocorticoid receptor expression. In addition, the inflammatory responses were suppressed in other types of cells. These results indicate the novel function of miR-766-3p, findings that may aid in the development of therapies to suppress inflammation, not only in RA but also in other diseases. [ABSTRACT FROM AUTHOR]