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Delayed wound healing is one of the severe complications after total ankle arthroplasty (TAA). In particular, once tibialis anterior (TA) tendon is exposed from tendon sheath of extensor retinaculum, wound healing will be critically intractable. We report three cases (mean age: 75.3 years old) of delayed wound healing after TAA cured by resection of TA tendon in patients with rheumatoid arthritis (RA). All three cases underwent TAA through an anterior approach, with careful suture of extensor retinaculum in wound closure. Ankle joint was fixed with splint and avoid weight bearing for three weeks after surgery. Delayed wound healing with TA tendon exposure was observed, and initially treated by debridement, basic fibroblast growth factor spray, and negative pressure wound therapy, which all failed to obtain wound healing. Finally, complete resection of TA tendon led to rapid wound healing. In all cases, ankle dorsal flexion was compensated by other extensors, with maintained range of motion and muscle strength (manual muscle testing 3 to 4) compared to pre-operation at 1 year after TAA operation. Resection of TA tendon may be considered as one of the salvage treatment options of severe delayed wound healing in TAA with anterior approach, especially in elderly patients. [ABSTRACT FROM AUTHOR]

Objective. It is often that patients with rheumatoid arthritis (RA) who require ankle surgeries already have the degeneration of talocalcaneal joints. When talocalcaneal joint was fused, whether operatively or spontaneously, ankle kinematics would be affected. The purpose of this paper was to study in vivo kinematics of mobile-bearing total ankle replacement (TAR) in rheumatoid ankle with concomitant talocalcaneal arthrodesis or with preexisting spontaneous talocalcaneal fusion. Methods. Thirteen TARs in ten patients with RA, in whom talocalcaneal joints had already been fused spontaneously or surgically, were studied. Fluoroscopic images were obtained while each patient was walking with full weightbearing on the implanted ankle. Thereafter tibio-talar motion was analyzed by 2D/3D registration technique. Results. Average tibio-talar motion was 4.0 ± 5.3° for plantarflexion and 6.6 ± 0.3° for dorsiflexion. Average range of internal/external rotation, inversion/eversion and AP translation was 3.8 ± 1.3°, 2.7 ± 1.0° and 1.6 ± 0.6 mm, respectively. Conclusions. Mobility of mobile-bearing TAR with talocalcaneal fusion was small during the stance phase of gait, but clinically measured ROM was mostly preserved. The movements of internal/external rotation and AP translation were allowed to a certain degree, but not of inversion/eversion. Even though the movement of inversion/eversion is limited, talocalcaneal arthrodesis could be accompanied with mobile-bearing TAR in rheumatoid ankles. [ABSTRACT FROM AUTHOR]

Objective. Plasmacytoid dendritic cells (pDCs) have been found to be accumulated in synovial tissues in rheumatoid arthritis (RA). Since pDCs originate from bone marrow (BM), we explored the differentiation of pDC in BM in RA and osteoarthritis (OA). Methods. BM mononuclear cells (BMMNCs) of the posterior ileac crest from 25 RA patients and 22 OA patients were examined for the expression of BDCA2 and CD34 by flow cytometry. The degree of synovial proliferation was assessed on light microscopy in 10 of 25 RA patients. Results. There were no significant differences in percentages of CD34 + cells or BDCA2 + cells within BMMNC between RA and OA. However, RA BMMNC contained higher percentages of BDCA2 + CD34 + cells (pre-pDCs) than OA BMMNCs. Accordingly, percentages of BDCA2 + CD34+ cells within BM CD34 + cells were significantly higher in RA than in OA. Finally, the percentages of BDCA2 + CD34+ cells within BM CD34 + cells were significantly correlated with the degree of synovial proliferation in RA. Conclusion. These results indicate that the generation of pre-pDC from BM CD34 + cells is increased in RA compared with OA. Moreover, the data suggest that the increased output of pDC from BM might be involved in the synovial proliferation in RA. [ABSTRACT FROM AUTHOR]

Anaerobic microbial activity has a major influence on the subsurface environment. We investigated the denitrification and methanogenesis in anoxic groundwater at a depth of 140 m in two boreholes drilled in a sedimentary geological setting, where the redox potential fluctuated. The average maximum potential denitrification rates, measured under anaerobic conditions in the two boreholes using an 15 N tracer, were 0.060 and 0.085 nmol 30N2 mL−1 h−1. The deduced NirS amino acid sequences obtained from in situ samples were similar to those of isolates belonging to the α-, β-, and γ- Proteobacteria, and the Firmicutes (72-100% similarity). Based on the nirS gene, the same operational taxonomic unit dominated incubated samples from each borehole. Methanogenesis candidates were detected by 16 S r RNA gene analysis, but no sequence was detected using primers for the functional methanogenesis gene mcrA. Although the stable isotope signatures suggested that some of the dissolved methane was of biogenic origin, no potential for methane production was evident during the incubations. The groundwater at 140 m depth did not contain oxygen, had an Eh ranging from −144 to 6.8 mV, and was found to be a potential field for denitrification. [ABSTRACT FROM AUTHOR]

Objectives: Vitamin K2 (VitK2) is reported to induce not only bone mineralization of human osteoblasts and apoptosis of osteoclasts, but also apoptosis of rheumatoid arthritis (RA) synovial cells, while its clinical effect on disease activity of RA remains unknown. Methods: 158 female RA patients (mean age 62.5 years) who had not been treated with warfarin, biologics, or teriparatide were enrolled in this study. VitK2 (45 mg/day) was administered in 70 patients with a serum undercarboxylated osteocalcin level of >4.5 ng/ml or with decreased bone mineral density in spite of the treatment with other anti-osteoporosis medications, regardless of RA disease activity. A longitudinal study was conducted in 52 patients who were additionally treated with VitK2 without changing their other medications for three months. Results: In the cross-sectional study, as compared to the VitK2-naïve group ( n = 88), the VitK2-treated group ( n = 70) showed lower serum CRP (1.7 ± 0.2 vs. 0.5 ± 0.1 mg/dl; P < 0.001), MMP-3 (220.4 ± 21.9 vs. 118.0 ± 14.4 ng/ml; P < 0.001), and DAS28-CRP (2.9 ± 0.1 vs. 2.4 ± 0.1; P < 0.05). In the longitudinal study, patients who were additionally treated with VitK2 showed significant decreases in serum CRP (1.1 ± 0.2 to 0.6 ± 0.2 mg/dl; P < 0.001), MMP-3 (160.1 ± 25.6 to 125.0 ± 17.8 ng/ml; P < 0.05), and DAS28-CRP (3.1 ± 0.2 to 2.4 ± 0.1; P < 0.001). Conclusions: VitK2 may have the potential to improve disease activity besides osteoporosis in RA. [ABSTRACT FROM AUTHOR]

Aim: The purpose of this study is to investigate the three-dimensional (3D) kinematics of preoperative osteoarthritic (OA) knees, and to clarify the validity of the findings in comparison with previous studies of kinematics in normal and OA knees. Materials and methods: Fifteen preoperative OA knees were scanned by 3D computed tomography (CT) at three positions. We created 3D bone models and quantitatively evaluated motion of the knee joint using a markerless volume-based registration technique. Assessment categories comprised rotation angles and anterior-posterior (AP) translation. The Pearson correlation test was used to analyze correlations between rotational angle and femorotibial angle. Results: From maximum extension to 90° flexion, 11 femurs displayed internal rotation relative to the tibia. In 10 knees, the sulcus moved >1 mm more backward than the lateral epicondyle. Significant differences were apparent between movement of the sulcus and lateral epicondyle. A correlation of −0.42 was found between the rotational angle and femorotibial angle. Conclusions: The kinematics of OA knees differed from that of normal knees in that femurs did not present external rotation with flexion. One reason for this movement is that the medial condyle of the femur tended to move backward in knee flexion due to disruption of the tibial joint surface. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to evaluate the clinical efficacy of monotherapy with alendronate and combined therapy with alendronate and menatetrenone (vitamin K2 [VitK2]) in postmenopausal rheumatoid arthritis (RA) patients with osteoporosis or osteopenia. Methods: Sixty-two postmenopausal RA patients with untreated osteoporosis or osteopenia (lumbar spine bone density ≤80 % of young adult mean [YAM]) were enrolled: 39 had abnormal serum undercarboxylated osteocalcin (ucOC) levels (>4.5 ng/mL) and received combined therapy with alendronate (35 mg/week) and VitK (45 mg/day) (ALN + K group); 23 had normal ucOC levels (≤4.5 ng/mL) and received alendronate monotherapy (35 mg/week) (ALN group). The clinical results for the 57 patients in both groups were evaluated after 1-year treatment. Results: The mean baseline/follow-up (FU) lumbar spine bone density (%YAM) values were 73.0/76.8 % ( P < 0.01) in the ALN + K group and 77.0/80.3 % ( P < 0.01) in the ALN group; a significant increase was shown in both groups. Mean proximal femoral bone density values at baseline/FU were 71.4/73.8 ( P < 0.01) in the ALN + K group and 71.4/71.6 % (not significant; NS) in the ALN group; a significant increase was shown in the ALN + K group only. Serum ucOC levels were normalized in the ALN + K group at FU. At FU, bone metabolism markers [bone-specific alkaline phosphatase (BAP) and N-terminal cross-linked telopeptides of type I collagen] were decreased in both groups. One patient in the ALN + K group and three in the ALN group suffered new fractures. Conclusions: Combined therapy with alendronate and VitK decreases bone metabolism marker levels and serum ucOC levels, and increases lumbar spine and femoral neck bone density in postmenopausal RA patients with abnormal ucOC levels and osteoporosis or osteopenia. [ABSTRACT FROM AUTHOR]

Objectives: Adalimumab, a fully human anti-tumor necrosis factor monoclonal antibody, was retrospectively evaluated for its effect on musculoskeletal manifestations and health-related quality of life in patients with psoriatic arthritis (PsA) during daily clinical practice. Methods: Patients who initiated adalimumab therapy after March 2010 were followed for at least 24 weeks with the clinical outcome measures. Eleven patients, all men with a mean age of 45.4 years, had mean psoriasis durations of 16.2 and 8.4 years at baseline. Results: After 24 weeks, 72.7, 63.6, and 45.5 % of the patients met the ACR 20, 50, and 70 response criteria, respectively, while 81.8 % achieved the PsA response criteria. Disease Activity Score using the 28-joint count and CRP declined from 3.2 ± 1.2 at baseline to 1.3 ± 0.4 at week 24 ( P < 0.01). The Bath Ankylosing Spondylitis Disease Activity Index and Bath Ankylosing Spondylitis Functional Index scores also decreased significantly (both P values were <0.01). After 24 weeks, three out of eight dimensions of the Medical Outcomes Study 36-Item Short Form Health Survey and Physical Component Summary were significantly improved (all P values were <0.05). Conclusions: Adalimumab exerted its effect as early as week 4, and it was sustained until the end of the 24-week observation period in the PsA patients. [ABSTRACT FROM AUTHOR]

We prospectively evaluated the effects of celecoxib (CEL) on the gastrointestinal (GI) tract of rheumatoid arthritis (RA) patients with endoscopically identified GI mucosal injury after therapeutic switching from the long-term use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Upper GI endoscopy was performed on RA patients who had been treated with NSAIDs for ≥3 months. GI mucosal injury was evaluated according to the modified LANZA score. Patients with mucosal injury without ulcers were switched from NSAIDs to CEL, while those with ulcers were switched to CEL with famotidine after ulcer healing. At week 16 of treatment, GI mucosal injury was endoscopically revaluated. An efficacy analysis was performed before therapeutic switching and at 8 and 16 weeks post-switching. Endoscopic analysis revealed GI mucosal injury, including six ulcers, in 45 of the 82 patients (54.9%). Sixteen weeks after switching to CEL, LANZA scores were significantly improved [2.1 ± 0.8 (pre-switching) vs. 1.6 ± 1.3, P = 0.0073] in patients with LANZA scores of 1, 2, or 3 ( n = 35). The Disease Activity Score using 28 joint counts (DAS28) [erythrocyte sedimentation rate item score (ESR4) ( P = 0.0257) and C-reactive protein item score (CRP4) ( P = 0.0031)] was also significantly improved by week 16. Based on these results, we conclude that preexisting NSAID-induced upper GI injury is improved following therapeutic switching to CEL without any reduction in analgesic efficacy. [ABSTRACT FROM AUTHOR]

Two cases of subcutaneous soft tissue infection in 30 RA patients treated with tocilizumab are reported. In both patients, local redness, swelling, and heat were observed around the affected site. WBC spikes and such local findings were suggested to be clinically useful for the early detection of low-grade subcutaneous infection in RA patients whose disease is tightly controlled with tocilizumab. Of note, the C-reactive protein (CRP) level and temperature lacked clinical utility for such detection. [ABSTRACT FROM AUTHOR]

One of the severe adverse effects of intra-articular injection in the knee is septic arthritis of the knee joint. Staphylococcus aureus is the most frequent pathogen of septic arthritis. Staphylococcal scalded skin syndrome (SSSS) refers to a spectrum of blistering skin diseases caused by S. aureus exfoliative toxins. Although SSSS is rarely observed in adults, the mortality rate is high in adult cases. We report a case of SSSS due to septic knee arthritis after intra-articular hyaluronic acid injections. [ABSTRACT FROM AUTHOR]

Our aim was to assess the ability of tocilizumab monotherapy to reduce progressive structural joint damage in rheumatoid arthritis patients at high risk of progression. This study was a subanalysis from a prospective 1-year, multicenter, X-ray-reader-blinded, randomized controlled trial of tocilizumab [Study of Active Controlled Monotherapy Used for Rheumatoid Arthritis, an IL-6 Inhibitor (SAMURAI) trial]. All patients were categorized into two or three groups according to four independent predictive markers for progressive joint damage [urinary C-terminal crosslinking telopeptide (uCTX-II), urinary pyridinoline/deoxypyridinoline (uPYD/DPD) ratio, body mass index (BMI), and joint-space narrowing (JSN) score at baseline]. One-year progression of joint destruction was assessed in high-risk versus low-risk groups receiving tocilizumab monotherapy and compared with patients receiving conventional disease-modifying antirheumatic drugs (DMARDs) ( n = 157 and 145, respectively). In patients at high risk of progression of erosion as estimated by high uCTX-II, uPYD/DPD, or low BMI, and at high risk of progression of JSN as estimated by low BMI or high JSN score, the 52-week changes in radiological erosion and JSN, respectively, were significantly less in patients treated with tocilizumab monotherapy compared with those receiving DMARDs for each type of risk factor. In patients at low risk, those receiving tocilizumab also progressed less than those on DMARDs, although the difference did not reach statistical significance. Tocilizumab monotherapy is more effective in reducing radiological progression in patients presenting with risk factors for rapid progression than in low-risk patients. Patients at high risk for progression may benefit more from tocilizumab treatment. [ABSTRACT FROM AUTHOR]

Synovial sarcoma (SS) is a malignant soft tissue tumor characterized by its unique t(X;18)(p11;q11) chromosomal translocation leading to the formation of the SS18-SSX fusion gene. The resulting fusion protein product is considered to play as an aberrant transcription factor and transform target cells by perturbing their gene expression program. However, the cellular origin of SS is highly debated. We herein established two novel human SS cell lines, named Yamato-SS and Aska-SS, and investigated their biological properties. We found the self-renewal ability of these cells to generate sarcospheres, to form tumors in serial xenotransplantation and reconstitute the tumor phenotypes without fractionation by any surface markers. Both SS cells as well as clinical tissue specimens from 15 patients expressed the marker genes-associated stem cell identity, Oct3/4, Nanog, and Sox2. We also found that both SS cells displayed limited differentiation potentials for mesenchymal lineages into osteocytes and chondrocytes albeit with the expression of early mesenchymal and hematopoietic lineage genes. Upon SS18-SSX silencing with sequence-specific siRNAs, these SS cells exhibited morphological transition from spherical growth in suspension to adherent growth in monolayer, additional expression of later mesenchymal and hematopoietic lineage genes, and broader differentiation potentials into osteocytes, chondrocytes, adipocytes, and macrophages in appropriate differentiation cocktails. Collectively, these data suggest that a human multipotent mesenchymal stem cell can serve as a cell of origin for SS and SS is a stem cell malignancy resulting from dysregulation of self-renewal and differentiation capacities driven by SS18-SSX fusion protein. STEM CELLS 2010;28:1119–1131 [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the predictive value of biological, radiological and clinical parameters for the progression of radiographic joint damage in rheumatoid arthritis (RA) patients treated with conventional disease-modifying anti-rheumatic drugs (DMARDs). We analyzed the 145 patients with active RA for less than 5 years who were participating in the prospective 1-year randomized controlled trial of tocilizumab (SAMURAI trial) as a control arm treated with conventional DMARDs. Progression of joint damage was assessed by sequential radiographs read by two independent blinded X-ray readers and scored for bone erosion and joint space narrowing (JSN) using the van der Heijde-modified Sharp method. Multivariate analysis revealed that increased urinary levels of C-terminal crosslinked telopeptide of type II collagen (U-CTX-II), an increased urinary total pyridinoline/total deoxypyridinoline (U-PYD/DPD) ratio and low body mass index (BMI) at baseline were independently associated with a higher risk for progression of bone erosion. In addition to these three variables, the JSN score at baseline was also significantly associated with an increased risk of progression of the JSN score and total Sharp score. High baseline U-CTX-II levels, U-PYD/DPD ratio and JSN score and a low BMI are independent predictive markers for the radiographically evident joint damage in patients with RA treated with conventional DMARDs. [ABSTRACT FROM AUTHOR]

In patients with rheumatoid arthritis (RA), juxta-articular intraosseous cystic lesions may cause spontaneous pathological fractures. The outcome of curettage and the packing of such lesions with interconnected porous calcium hydroxyapatite ceramic (IP-CHA) was investigated. Twelve lesions were treated in ten RA patients (three men and seven women with a mean age of 59 years). Ten lesions were associated with impending pathological fracture involving the articular surface. In all patients, curettage and packing of the bone cavity with IP-CHA were done. Assessment was based on final radiographs obtained an average of 30 months after surgery (range 10–47 months). Absorption of the implanted IP-CHA, expansion of the lesion, implant incorporation into host bone, and postoperative fractures were investigated. At final follow-up, there was no absorption of the implanted IP-CHA in any of the lesions. Expansion of the radiolucent area was only noted in one lesion. Seven of the other 11 lesions showed major incorporation of IP-CHA into host bone, while minor incorporation was seen in four lesions. There were no postoperative fractures. In conclusion, curettage and packing with IP-CHA is a feasible method of preventing pathological fracture due to juxta-articular intraosseous cystic lesions in RA patients. [ABSTRACT FROM AUTHOR]

We examined a new-generation yttria-stabilized zirconia head manufactured by NGK 1 year after total hip arthroplasty. Monoclinic content of the retrieved head was twice that of the unused head at the pole and equator. A fourfold increase in monoclinic content was observed at 5 mm below the equator. Transformation from the tetragonal phase to the monoclinic phase occurred in the new generation zirconia with alumina doping within a relatively short period in vivo. [ABSTRACT FROM AUTHOR]

To examine the clinical features of vertebral and non-vertebral fractures in patients with rheumatoid arthritis (RA), including insufficiency fractures, and to assess the risk factors for fracture, we prospectively studied 209 outpatients with rheumatoid arthritis for 1 year. The age, gender, Steinbrocker’s functional class, glucocorticoid use, history of lower limb surgery, serum C-reactive protein (CRP), and use of bisphosphonates were evaluated. Examination for fractures was performed by radiography, computed tomography (CT), magnetic resonance imaging (MRI), and bone scanning. Thirty-three fractures occurred in 24 patients over the 1-year study period, and the incidence was 15.8 fractures per 100 patient-years. Fractures occurred at various sites. The majority (70%) was insufficiency fracture, and more than 50% caused ambulatory dysfunction. Radiographic findings were absent in 39% of the fractures at the onset of pain. The functional class and glucocorticoid dose were significantly associated with fracture development. This prospective study showed that the incidence of fractures, especially insufficiency fractures, was very high in patients with rheumatoid arthritis and that most of their fractures caused gait disturbance. Early intervention to prevent secondary osteoporosis is recommended to maintain the quality of life in patients with rheumatoid arthritis, especially those with functional impairment or undergoing glucocorticoid therapy. [ABSTRACT FROM AUTHOR]

Previous studies demonstrated the existence of osteoblastic cells in circulating blood. Recently, we reported that osteoblast progenitor cells (OPCs) in circulation originated from bone marrow and contributed to the formation of ectopic bone induced by implantation of a bone morphogenetic protein (BMP)-2-containing collagen pellet in mouse muscular tissue. However, the character of circulating bone marrow-derived osteoblast progenitor cells (MOPCs) and the precise mechanisms involving the circulating MOPCs in the osteogenic processes, such as signals that recruit the circulating MOPCs to the osseous tissues, have been obscure. In this report, we demonstrated for the first time that the MOPCs were mobilized from intact bones to transiently occupy approximately 80% of the mononuclear cell population in the circulating blood by BMP-2- pellet implantation. The mobilized MOPCs in the circulation did not express the hematopoietic marker CD45 on their surface, but they expressed CD44 and CXCR4, receptors of osteopontin and stromal cell-derived factor-1 (SDF-1), respectively. The MOPCs isolated from the mouse peripheral blood showed the ability to be osteoblasts in vitro and in vivo. Furthermore, the MOPCs in the circulation efficiently migrated to the region of bone formation by chemoattraction of SDF-1 expressed in vascular endothelial cells and the de novo osteoblasts of the region. These data may provide a novel insight into the mechanism of bone formation involving MOPCs in circulating blood, as well as perspective on the use of circulating MOPCs to accelerate bone regeneration in the future. [ABSTRACT FROM AUTHOR]

The effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on juxta-articular osteopenia and growth plate destruction adjacent to inflamed joints was investigated in rats with collagen-induced arthritis. Forty rats were assigned to the following six groups: (1) an untreated arthritis group; (2–5) arthritis rats receiving indomethacin (3 mg/kg per day), dexamethasone (0.2 mg/kg per day), or celecoxib (5 or 50 mg/kg per day), and (6) normal control rats. Drugs were administered for 2 weeks from the onset of arthritis. Then the hind paws were measured. Juxta-articular osteopenia and growth plate destruction adjacent to inflamed joints were also assessed using plain radiography, bone mineral density measurement, histology, and histomorphometry. Each treatment reduced inflammation, but only dexamethasone and high-dose celecoxib prevented bone loss adjacent to inflamed joints and significantly decreased bone resorption. In contrast, no treatment affected bone formation parameters. Growth plate destruction adjacent to inflamed joints was prevented by indomethacin, dexamethasone, and high-dose celecoxib. Although dexamethasone abolished inflammation, growth plate destruction was still observed. In conclusion, among the various drugs tested, only celecoxib had a preventive effect on both growth plate destruction and bone loss adjacent to inflamed joints in this arthritis model. [ABSTRACT FROM AUTHOR]

The efficacy of two different cationic liposomes, Lipofectin and hemagglutinating virus of Japan (HVJ)-cationic liposomes, on nuclear uptake of fluorescence-labeled phospho-rothioate oligodeoxyribonucleotide (S-ODN) by ligament scar fibroblasts and suppression of decorin mRNA expression when antisense decorin S-ODN was transferred was investigated. There was no significant difference in nuclear uptake of fluorescent ODN between the two methods. However, only HVJ-cationic liposomes had a significant effect on suppression of decorin mRNA expression levels. To address the discrepancy, the molecular integrity of the transferred ODN in the cells was assessed by analysis of fluorescence resonance energy transfer (FRET) within double-fluorescence-labeled S-ODN. More than 70% of the ODN transfected by HVJ-cationic liposomes remained intact within the nucleus at 20 h after transfection, while the majority of the ODN transferred by Lipofectin was degraded at this point. These results suggest a strong relationship between the nuclear integrity of transfected antisense ODN and its suppression of target mRNA expression. [ABSTRACT FROM AUTHOR]

We purified and characterized glutaredoxin (thioltransferase), which catalyzes thiol/disulfide exchange reaction, for the first time in plants. The purification procedure employed an immunoabsorbent, antiglutaredoxin-Sepharose. Glutaredoxin was purified about 2,200-fold from rice bran and it appeared to be homogeneous on SDS-PAGE. MALDI-TOF mass spectrometry revealed that the protein has a molecular mass of 11,097.9 Da. Rice glutaredoxin consists of 105 amino acid residues, containing the tetrapeptide-Cys-Phe-Pro (Tyr)-Cys-, which constitutes the active site of Escherichia coli and mammalian glutaredoxins. Inactivation assay also indicated that cysteine residues are responsible for enzyme activity. Kinetic analyses revealed that the enzyme did not exhibit normal Michaelis-Menten kinetics. The enzyme has an optimum pH of about 8.7 with 2-hydroxyethyl disulfide as a substrate. In addition, rice glutaredoxin has dehydroascorbate reductase activity, like mammalian glutaredoxin. [ABSTRACT FROM AUTHOR]

Objective. To evaluate the osteoblastic differentiation of human mesenchymal stem cells (hMSCs) in patients with RA. Methods. Heparinized bone marrow aspirate was obtained from patients with OA and RA. Mononuclear cells were cultured for 2 weeks and a colony-forming assay was performed. The phenotype of cells was analysed by flow cytometry. Passage 2 cells were cultured with β-glycerophosphate (bGP) in the control group and bGP, ascorbic acid and dexamethasone in the differentiation group. After 2 weeks, ALP staining and activity were performed. After 3 weeks, Alizarin Red S assay was performed. Total RNA was extracted from cells cultured for 2 and 3 weeks. Gene expression of bone formation factor was examined by real-time PCR. Results. The phenotype of cells was identical in both OA and RA and the content was thought to be hMSCs. The results of ALP activity and Alizarin Red S assay showed higher levels in the differentiation group for both OA and RA samples compared with the control group. The results of a colony-forming assay were identical in both OA and RA samples. Gene expression in the differentiation group was higher than in the control group in both OA and RA samples. There was no significant difference between OA and RA samples in all experiments. Conclusion. The function of osteoblastic differentiation of hMSCs is similar between OA and RA. [ABSTRACT FROM AUTHOR]