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Supplementary Figure 1.

Rhabdoid tumor is an aggressive, early childhood tumor. Biallelic inactivation of the SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1)/integrase interactor 1 (INI1) gene is the only common genetic feature in rhabdoid tumors. Loss of SMARCB1 function results in downregulation of several tumor suppressor genes including p16, p21, and NOXA. The novel histone deacetylase inhibitor, OBP-801, induces p21 and has shown efficacy against various cancers. In our study, OBP-801 strongly inhibited the cell growth of all rhabdoid tumor cell lines in WST-8 assay. However, Western blotting and cell-cycle analysis revealed that OBP-801 did not activate the P21-RB pathway in some cell lines. p21 knockout indicated that p21 did not dominate the OBP-801 antitumor effect in rhabdoid tumor cell lines. We discovered that OBP-801 induced NOXA expression and caspase-dependent apoptosis in rhabdoid tumor cell lines independent of TP53. Chromatin immunoprecipitation assay showed that OBP-801 acetylated histone proteins and recruited RNA polymerase II to the transcription start site (TSS) of the NOXA promotor. Moreover, OBP-801 recruited BRG1 and BAF155, which are members of the SWI/SNF complex, to the TSS of the NOXA promotor. These results suggest that OBP-801 epigenetically releases the silencing of NOXA and induces apoptosis in rhabdoid tumors. OBP-801 strongly inhibited tumor growth in human rhabdoid tumor xenograft mouse models in vivo. Terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling and cleaved caspase-3 were stained in tumors treated with OBP-801. In conclusion, OBP-801 induces apoptosis in rhabdoid tumor cells by epigenetically releasing the silencing of NOXA, which is a key mediator of rhabdoid tumor apoptosis. The epigenetic approach for NOXA silencing with OBP-801 is promising for rhabdoid tumor treatment.

Supplementary Figure 3.

Supplementary table

Supplementary Figure 2.

Patients with high-risk neuroblastoma have a poor prognosis; new therapeutic agents are therefore required. We investigated the antitumor effects of OBP-801, a novel histone deacetylase inhibitor, its underlying mechanism, and its potential as a therapeutic agent for patients with neuroblastoma.The study included five human neuroblastoma cell lines: IMR32, GOTO, KP-N-RTBM, SK-N-AS, and SH-SY5Y. We investigated cell proliferation, cell cycle status, protein expression patterns, and apoptosis in neuroblastoma cells after OBP-801 treatment in vitro. Cell survival rate and cell cycle were analyzed using the WST-8 assay and flow cytometry, respectively. Apoptosis was detected using annexin V staining, and the expression of apoptosis-related proteins was investigated by western blotting. The antitumor activity of OBP-801 was examined in an in vivo xenograft mouse model.Dose-effect curve analysis showed that the mean half-maximal inhibitory concentration value was 5.5 ± 5.9 nM for the MYCN-amplified cell lines (IMR32, GOTO, and KP-N-RTBM) and 3.1 ± 0.7 nM for the MYCN-nonamplified cell lines (SK-N-AS and SH-SY5Y). OBP-801 inhibited cell proliferation and growth in all the cell lines. It induced G2/M phase arrest through the p21 (CDKN1A) pathway, increasing histone H3 levels and, subsequently, apoptosis in human neuroblastoma cells. OBP-801 suppressed the growth of neuroblastoma cells in the mouse xenograft model.Overall, OBP-801 induces M-phase arrest and apoptosis in neuroblastoma cells via mitotic catastrophe. Our results indicate that OBP-801 is a promising therapeutic agent with fewer adverse effects for patients with neuroblastoma.

We investigated the effects of adipose-derived extract (AE) on cultured chondrocytes and in vivo cartilage destruction. AE was prepared from human adipose tissues using a nonenzymatic approach. Cultured human chondrocytes were stimulated with interleukin-1 beta (IL-1 beta) with or without different concentrations of AE. The effects of co-treatment with AE on intracellular signaling pathways and their downstream gene and protein expressions were examined using real-time PCR, Western blotting, and immunofluorescence staining. Rat AE prepared from inguinal adipose tissues was intra-articularly delivered to the knee joints of rats with experimental osteoarthritis (OA), and the effect of AE on cartilage destruction was evaluated histologically. In vitro, co-treatment with IL-1 beta combined with AE reduced activation of the p38 and ERK mitogen-activated protein kinase (MAPK) pathway and nuclear translocation of the p65 subunit of nuclear factor-kappa B (NF-kappa B), and subsequently downregulated the expressions of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, IL-6, and IL-8, whereas it markedly upregulated the expression of IL-1 receptor type 2 (IL-1R2) in chondrocytes. Intra-articular injection of homologous AE significantly ameliorated cartilage destruction six weeks postoperatively in the rat OA model. These results suggested that AE may exert a chondroprotective effect, at least in part, through modulation of the IL-1 beta-induced inflammatory signaling pathway by upregulation of IL-1R2 expression.

We investigated the expression and localization of the receptor activator nuclear factor κB ligand (RANKL) in cartilage from patients with rheumatoid arthritis (RA) of relevance to cartilage degeneration. We also examined the role of exogenous lymphotoxin (LT)-α on RANKL expression in human chondrocytes and its effect on in vitro osteoclast differentiation. Cartilage and synovial fluid samples were obtained from 45 patients undergoing total joint replacement surgery or joint puncture, including 24 patients with osteoarthritis (OA) and 21 patients with RA. RANKL expression in articular cartilage was examined by immunohistochemistry. LT-α concentrations in synovial fluid were measured using an enzyme-linked immunosorbent assay (ELISA). Normal human chondrocytes were stimulated with LT-α, and the relative mRNA levels of RANKL, osteoprotegerin (OPG), matrix metalloproteinase-9, and vascular endothelial growth factor were examined by real-time polymerase chain reaction. Soluble RANKL protein in culture media was measured using ELISA, and membrane-bound RANKL protein in cells was examined by western blotting. Co-cultures of human chondrocytes with peripheral blood mononuclear cells (PBMCs) were stimulated with macrophage-colony stimulating factor and LT-α, and osteoclast differentiation was evaluated by staining for tartrate-resistant acid phosphatase. LT-α concentrations were higher in RA synovial fluid than in OA samples. The population of RANKL-positive chondrocytes of RA cartilage was higher than that of OA cartilage, and correlated with cartilage degeneration. Stimulation of cultured human chondrocytes by LT-α increased RANKL expression, the RANKL/OPG ratio, and angiogenic factors. Membrane-bound RANKL in chondrocytes was up-regulated after stimulation of LT-α, whereas soluble RANKL in culture medium did not increase. Co-cultures of human chondrocytes and PBMCs demonstrated that LT-α stimulated human chondrocytes to produce RANKL and induced osteoclastic differentiation of PBMCs. RANKL produced by chondrocytes may contribute to cartilage destruction during RA and LT-α could promote the expression of RANKL in human chondrocytes.

We investigated the clinical outcomes of surgical procedures for the treatment of forefoot deformities in patients with rheumatoid arthritis. Twenty feet in 16 women (mean age 62.1 years) underwent corrective osteotomy of the first metatarsal bone with shortening oblique osteotomy of the lesser metatarsophalangeal joints (joint-preservation group), while 13 feet in 12 women (mean age 67.4 years) underwent arthrodesis of the first metatarsophalangeal joint with resection arthroplasty of the lesser metatarsophalangeal joints (joint-sacrifice group); mean follow-up for each group was 25.8 and 23.8 months, respectively. The mean total Japanese Society for Surgery of the Foot (JSSF) scale improved significantly from 64.2 to 89.2 in the joint-preservation group (p.001), and from 54.2 to 74.2 in the joint-sacrifice group (p = .003). In the joint-preservation group, the postoperative range of motion (ROM) of the joint, walking ability, and activities of daily living scores of the JSSF scale were significantly higher than those in the joint-sacrifice group (p = .001, p = .001, and p = .019, respectively). There were no differences in the subscale scores of the self-administered foot evaluation questionnaire between 2 groups either pre- or postoperatively. No differences in the postoperative complications were found between 2 groups. Although the joint-sacrificing procedure resulted in lower objective outcomes than the joint-preserving procedure regarding the ROM of the joint, the walking ability, and the level of activities of daily living, both procedures resulted in similar treatment outcomes when evaluated by the subjective measures.

Rhabdoid tumor is an aggressive, early childhood tumor. Biallelic inactivation of the SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1)/integrase interactor 1 (INI1) gene is the only common genetic feature in rhabdoid tumors. Loss of SMARCB1 function results in downregulation of several tumor suppressor genes including p16, p21, and NOXA. The novel histone deacetylase inhibitor, OBP-801, induces p21 and has shown efficacy against various cancers. In our study, OBP-801 strongly inhibited the cell growth of all rhabdoid tumor cell lines in WST-8 assay. However, Western blotting and cell-cycle analysis revealed that OBP-801 did not activate the P21-RB pathway in some cell lines. p21 knockout indicated that p21 did not dominate the OBP-801 antitumor effect in rhabdoid tumor cell lines. We discovered that OBP-801 induced NOXA expression and caspase-dependent apoptosis in rhabdoid tumor cell lines independent of TP53. Chromatin immunoprecipitation assay showed that OBP-801 acetylated histone proteins and recruited RNA polymerase II to the transcription start site (TSS) of the NOXA promotor. Moreover, OBP-801 recruited BRG1 and BAF155, which are members of the SWI/SNF complex, to the TSS of the NOXA promotor. These results suggest that OBP-801 epigenetically releases the silencing of NOXA and induces apoptosis in rhabdoid tumors. OBP-801 strongly inhibited tumor growth in human rhabdoid tumor xenograft mouse models in vivo. Terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling and cleaved caspase-3 were stained in tumors treated with OBP-801. In conclusion, OBP-801 induces apoptosis in rhabdoid tumor cells by epigenetically releasing the silencing of NOXA, which is a key mediator of rhabdoid tumor apoptosis. The epigenetic approach for NOXA silencing with OBP-801 is promising for rhabdoid tumor treatment.

Seronegative myasthenia gravis (MG) is a generalized form of MG that is diagnosed on the basis of clinical symptoms, electrophysiological testing, and pharmacological responses, in the absence of a seropositive status for anti-acetylcholine receptor (AChR) antibodies. Generalized MG that is seronegative for anti-AChR, anti-muscle-specific kinase (MuSK), and anti-low density lipoprotein receptor related protein 4 (Lrp4) antibodies is known as triple-seronegative MG. We here describe a case of triple-seronegative MG in an 8-year-old boy. His first symptom was dysphagia, at 3 years of age, and he subsequently developed ptosis, rhinolalia, and a waddling gait. A genetic analysis was conducted to exclude the possibility of congenital myasthenia syndrome due to the patient's resistance to steroid therapy. His condition was successfully managed with tacrolimus therapy over a 5-year follow-up period. Recently, several studies have reported the therapeutic utility of tacrolimus in juvenile seropositive MG; in contrast, a few reports have described tacrolimus treatment in cases of seronegative MG. Our findings suggest that tacrolimus therapy is a safe and effective option for the treatment of juvenile seronegative MG.

To investigate whether janus kinase (JAK) inhibitor exhibits a chondro-protective effect against mechanical stress-induced expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and matrix metalloproteinase (MMPs) in human chondrocytes. Normal human articular chondrocytes were seeded onto stretch chambers and incubated with or without tofacitinib (1000 nM) for 12 h before mechanical stimulation or cytokine stimulation. Uni-axial cyclic tensile strain (CTS) (0.5 Hz, 10% elongation, 30 min) was applied and the gene expression levels of type II collagen α1 chain (COL2A1), aggrecan (ACAN), ADAMTS4, ADAMTS5, MMP13, and runt-related transcription factor 2 (RUNX-2) were examined by real-time polymerase chain reaction. Nuclear translocation of RUNX-2 and nuclear factor-κB (NF-κB) was examined by immunocytochemistry, and phosphorylation of mitogen-activated protein kinase (MAPK) and signaling transducer and activator of transcription (STAT) 3 was examined by western blotting. The concentration of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in the supernatant was examined by enzyme-linked immunosorbent assay. COL2A1 and ACAN gene expression levels were decreased by CTS, but these catabolic effects were canceled by tofacitinib. Tofacitinib significantly down-regulated CTS-induced expression of ADAMTS4, ADAMTS5, MMP13, and RUNX2, and the release of IL-6 in supernatant by chondrocytes. Tofacitinib also reduced CTS-induced nuclear translocation of RUNX-2 and NF-κB, and phosphorylation of MAPK and STAT3. Tofacitinib suppressed mechanical stress-induced expression of ADAMTS4, ADAMTS5, and MMP13 by human chondrocytes through inhibition of the JAK/STAT and MAPK cascades.

Rhabdomyosarcoma (RMS) is an aggressive pediatric cancer of musculoskeletal origin. Despite multidisciplinary approaches, such as surgical resection, irradiation, and intensive chemotherapy, adopted for its treatment, the prognosis of patients with high‑risk RMS remains poor. Thus, molecularly targeted therapies are required to improve patient survival and minimize side effects. Histone deacetylases (HDACs) modify transcription by deacetylation of the lysine residues in chromatin histone tails and several non‑histone proteins. HDAC inhibitors, classes of compounds targeted to various HDAC proteins, are being studied for their roles in several types of cancers in a rigorous manner. This study aimed to investigate the potential of a novel HDAC inhibitor, OBP‑801, as a therapeutic agent for the treatment of RMS. We used 8 RMS cell lines in this study. Protein expression patterns, cell proliferation, cell cycle status, and apoptosis in RMS cells after OBP‑801 treatment in vitro were investigated. We also studied the antitumor activity of OBP‑801 in an in vivo xenograft mouse model. We observed cell cycle arrest at the M‑phase and apoptosis in all RMS cell lines after exposure to pharmacological levels of OBP‑801 for 24 h. Immunofluorescence staining revealed that OBP‑801 may induce mitotic catastrophe via chromosome misalignment and reduced survivin expression, ultimately leading to apoptosis. Our results demonstrated that the novel HDAC inhibitor OBP‑801 was an effective inhibitor of RMS cell line proliferation and may be a potent therapeutic option for RMS.

Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases.

Swyer-James syndrome is a rare syndrome that occurs as a result of repeated bronchiolitis and pneumonitis in childhood. Most cases are asymptomatic, and subsequent diagnosis may not occur until adulthood. We present the case of a 7-year-old female with Swyer-James syndrome, which was initially diagnosed and treated as asthma. The patient developed respiratory distress and atelectasis which were treated with biphasic cuirass ventilation. This case suggests that Swyer-James syndrome should be a concern in patients with chronic cough and wheezing, and highlights the importance of taking a careful history and appropriate radiological investigations for diagnosis. Once Swyer-James syndrome is diagnosed, prophylaxis and appropriate management of respiratory infections becomes important.

Ulnar neuropathy is one of complications of TEA (total elbow arthroplasty, incidence; 5 to 10%), yet there are not many evaluations and clinical course reports. Out of 117 patients with rheumatoid arthritis (RA) who underwent TEA, 8 patients showed numbness and muscle weakness of the ulnar nerve region after surgery, and received electromyography (EMG). EMG examinations revealed ulnar neuropathy at the elbow in 6 subjects, 5 of whom performed neurolysis. Two patients were diagnosed with cervical spondylosis. A 50-year-old female developed RA in 1998. She underwent left TEA (JACE) in June 2014. As numbness appeared, we performed EMG to her in October 2014. Delay of sensory nerve conduction velocity (SCV) was observed at cubital tunnel. In April 2015 left ulnar nerve neurolysis was performed. After that, both EMG finding and symptoms were improved. However, EMG in June 2016 again confirmed a delay in SCV and we performed a second ulnar nerve neurolysis in September 2016. Evaluations of ulnar neuropathy are important because RA also causes cervical spinal lesions such as atlantoaxial subluxation. Adhesion and scars are recognized at the elbow joint in the five patients who underwent neurolysis. Thus, it is necessary to follow up with electromyogram examination, for diagnosis of neuropathy and postoperative evaluation.

Background Treatment of rheumatoid arthritis (RA) has improved over the past decade with the modification of treatment strategy and recent application of biologic agents (Bio). It has been revealed that the treatment by Bio achieved not only improvement of clinical symptom, but also inhibition of the progression of joint destruction in small joints of hand and foot. However, there are little evidences of inhibition of the progression of the large joint destruction with the treatment by Bio. ARASHI score, is composed of ARASHI Status Score (ASS) and ARASHI Change Score (ACS), and have been newly developed to evaluate the progression of the large joint destruction as well as remodeling 1) Objectives We aimed to investigate the correlation among the ARASHI score, modified total sharp score (mTSS), and other clinical parameters, and to clarify the patients9 parameters leading to large joint destructions in patients with RA under disease control by Bio. Methods 75 patients with RA under disease control by Bio were available for the current study. Average patients9 age, disease duration, and follow-up periods were 62.6 (years old), 11.7 (year), and 21.8 (month), respectively. They were examined for serum level of C-reactive protein (CRP), mHAQ, DAS28-CRP, SDAI, CDAI, mTSS, and ASS at the beginning of the study. The amount of change of CRP, mHAQ, DAS28-CRP, SDAI, CDAI, and mTSS at the final follow-up were defined as ΔCRP, ΔmHAQ, ΔDAS28-CRP, ΔSDAI, ΔCDAI, and ΔmTSS, respectively. Statistical analysis was performed by Spearman9s correlation co-efficient. Results Average ΔCRP, ΔmHAQ, ΔDAS28-CRP, ΔSDAI, ΔCDAI, ΔmTSS, and ACS were 0.01, -0.02, -0.28, -2.62, -2.64, and 0.03, respectively. There was no significant correlation between the ACS and ΔmTSS. There were no significant correlations between ΔmTSS and other clinical parameters, whereas ACS was significantly correlated with ΔCRP (r=0.39), ΔmHAQ (r=0.28), ΔDAS28-CRP (r=0.39), ΔSDAI (r=0.35), and ΔCDAI (r=0.32). Conclusions The correlation between the destruction of small joints of hands and feet and the disease activity was not seen among the current patients group with long-standing disease. In contrast, our results suggested that sufficient suppression of the disease activity is important to prevent the progression of large joint destruction among long-standing RA patients under control by Bio. References Kaneko A, et al., Mod Rheumatol. 2013;23:1053–62 Disclosure of Interest None declared

Background The goal of treat to target (T2T) is the clinical remission in patients with early disease, but it is difficult to achieve the functional remission. Although patient9s subjective evaluation is important for the assessment of postoperative functions of rheumatoid arthritis (RA) patients, there are few reports examined the patients-reported functions after upper extremity surgery for RA. Objectives Between 2011 and 2014, 158 RA patients underwent the surgical treatment on upper extremities, and all patients were available for detailed clinical review over a 1-year follow-up period. There were 144 females and 14 males with a mean age at surgery of 59.7 (range, 18–85) years. The average disease duration at the surgery was 19.6 (range, 1–59) years. Methods The clinical outcome of the surgery was assessed by the disease activity (DAS28-CRP), Health Assessment Questionnaire Disability Index (HAQ-DI), Disability of Arm Shoulder and Hand (DASH), Hand20 questionnaire (Hand20). The patients were divided by surgical site into 3 groups (elbow, wrist and finger groups) and by the use of biological disease-modifying anti-rheumatic drugs (bDMARDs) into 2 groups (bDMARDs and non-bDMARDs groups) to compare and evaluate the outcomes. Results The mean of preoperative/postoperative DAS28-CRP, HAQ-DI, DASH and Hand20 were 2.9/2.3, 0.88/0.94, 46.4/39.1 and 59.1/47.6, respectively. All outcomes except for HAQ-DI significantly improved after the surgery. All outcomes improved significantly in the elbow group, but could not reach significant improvement in the finger group. We further examined the postoperative change in each items of DASH and Hand20, and found the significant improvements in items about pain and weakness in elbow group, pain and rotation of forearm in wrist group, and delicate movement and cosmetic factor in finger group. Postoperative DASH and Hand20 scores were tend to improve in the both bDMARDs and non-bDMARDs group. Conclusions Our results confirmed the surgery on upper extremity of RA improved the patient9s reported function, as well as the disease activity. There were surgical site-specific pattern of improvement of DASH and Hand20, such as that gross movement and pain significantly improved in larger joints, and dexterity movement and cosmetic factor in smaller joints. Postoperative upper extremity function was tend to improve, but more significantly in non-bDMARDs group, probably because the patients might had relatively better baseline function in the bDMARDs group. Understanding of site-specific patterns of improvement after surgery might be useful to achieve the functional remission, and may contribute to decision making of surgical indication, priority of surgical site on upper extremity, and prospection of surgical outcome. References Moromoto H, et al. Reliability of the Hand20 questionnaire: comparison with the 36-Item Short-Form Health Survey. Hand Surg. 2014;19(1):1–6 Hudak PL, et al. Development of an upper extremity outcome measure: the DASH (disabilities of the arm, shoulder and hand) [corrected]. The Upper Extremity Collaborative Group (UECG). Am J Ind Med. 1996 Jun;29(6):602–8. Disclosure of Interest None declared

Background Patient self-administered questionnaires remove the possibility of observer bias, and are important instruments for the assessment of clinical outcome. The patient-rated elbow evaluation (PREE) is a joint-specific, self-administered questionnaires. Objectives We aimed to investigate the correlation between the Japanese version of PREE (PREE-J) and other clinical parameters in rheumatoid arthritis (RA) patients before and after total elbow arthroplasty (TEA). Methods Thirty-five elbows in 32 RA patients (M/F: 3/29) were replaced by TEA. The mean age was 62.1 (range 41–79) years at the time of surgery, the mean follow-up period was 21.5 (range 12–36) months. All patients were assessed pre- and post-operatively by PREE-J, elbow and forearm range of motion (ROM), Disease Activity Score with 28 joint using CRP (DAS28-CRP), Mayo Elbow Performance Score (MEPS), Japanese version of the Disabilities of the Arm, Shoulder and HAND (DASH-JSSH) and Health Assessment Questionnaire Disability Index (HAQ-DI). The changes of parameters after surgery were examined by Wilcoxon signed-rank test, and the correlation between PREE-J and other parameters was examined using Spearman9s correlation coefficients. Results Both pre- and post-operative PREE-J significantly correlated with DAS28-CRP, DASH-JSSH, and HAQ-DI. Significant improvement was observed after surgery in all parameters except for HAQ-DI. The mean postoperative MEPS improved from 50.3±16.4 points to 98.1±3.2 points, the average postoperative PREE-J improved from 54.7±19.3 points to 27.1±24.4 points. The correlation between PREE-J and MEPS was significant preoperatively (p Conclusions The current study indicated that elbow evaluation by patients who underwent TEA showed significant correlation with disease activity, upper limb function and disability in daily life. It was revealed preoperative PREE-J also well correlated with MEPS, which is widely accepted evaluation system by elbow surgeons. Interestingly, PREE-J did not correlate with MEPS and ROM postoperatively. As PREE-J contains many questions about complex motions required the multiple joint function of upper extremity, it is possible PREE-J might be influenced by other joints affected by RA. MEPS (up to 100 points) evaluates pain (45), ROM (20), function (25) and instability (10) of the elbow, and reached almost perfect score by TEA. PREE-J evaluates pain and function with more detailed questionnaires than MEPS, some of them cannot be solved by a single joint surgery. Our results suggested PREE-J might be useful and wide range evaluation instrument for functional improvement of upper extremity after TEA. Disclosure of Interest None declared

Background Recent effective treatment with disease-modifying anti-rheumatic drugs (DMARDs) including biologic DMARDs (bDMARDs) improved the disease control of patients with rheumatoid arthritis (RA), and the change of body image of the patients might influenced the surgical indication. Body image assessment tool (BIAT) has been reported to be a reliable and valid tool1). Patients with RA had a worse body image than individuals without RA2), however, there are no evidence showed the body image of patients who requires surgical intervention. Objectives The current study aimed to investigate the body image of patients who requires surgical intervention and to examine the correlation with depressive condition. Methods 163 patients (16 male, 147 female) with RA were divided into two groups of patients who didn9t require the surgical intervention (non-operative group) and who underwent surgery (operative group). The non-operative group and operative group included 88 and 75 patients, respectively. The mean age of the non-operative and operative group were 64.8 and 64.4 years, and the mean disease duration were 17.5 and 22.7 years, respectively. The clinical evaluation included the use of bDMARDs, pain VAS (0–100mm), Health Assessment Questionnaire Disability Index (HAQ-DI), disease activity (DAS28-CRP), depression assessed by Beck Depression Inventory-II (BDI-II), and body image assessed by BIAT. Statistical analyses were performed using the Mann-Whitney U test, and Fisher9s exact test. Results The rate of use of bDMARDs was not significant between non-operative and operative group. In the operative group, pain VAS, HAQ-DI, DAS28-CRP and BDI-II were significantly higher (p Conclusions The result of this survey found the body image of patients in operative group was disturbed than that of non-operative patients. Body image disturbance was highly correlated with depressive condition in both operative and non-operative patients. To assess the body image might be useful to understand the patients9 expectation and proper indication of the surgery. References Fujisaki K. Issues in nursing research of body image. Kango Kenkyu, 1996; 29 (4):307–319. Jorge RT, et al. Body image in patients with rheumatoid arthritis. Mod Rhematol, 2010; 20(5): 491–495. Disclosure of Interest None declared