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Background: Total hip arthroplasty (THA) has been highlighted as the best treatment option for ankylosing spondylitis (AS) patients with advanced hip involvement. The huge blood loss associated with THA is a common concern of postoperative complications. Disease activity is a specific reflection of systematic inflammation of AS. The purpose of this study was to determine the effect of disease activity on blood loss during THA in patients with AS. Methods: Forty-nine patients with AS who underwent unilateral THAs were retrospectively studied. Ankylosing Spondylitis Disease Activity Score (ASDAS) was employed to evaluate the disease activity. Orthopedic Surgery Transfusion Hemoglobin European Overview (OSTHEO) formula was used to assess the surgical blood loss. The patients were divided into active group (ASDAS≥1.3; n = 32) and stable groups (ASDAS< 1.3; n = 17) based on the ASDAS. Peri-operative laboratory values, plain radiographs, intra-operative data, transfusion volume, and use of hemostatic agents were recorded and statistically analyzed. Results: The ASDAS, pre-operative C-reactive protein level, erythrocyte sedimentation rate, and fibrinogen concentration in the active group were higher than the stable group (all P < 0.05); however, the pre-operative hemoglobin concentration and albumin level were higher in the stable group (both P < 0.05). The total blood loss during THA in stable patients was 1415.31 mL and 2035.04 mL in active patients (P = 0.006). The difference between the two groups was shown to be consistent after excluding the gender difference (P = 0.030). A high transfusion rate existed in both groups (stable group, 76.47% with an average of 1.53 units; active group, 84.37% with an average of 2.31 units), but there was no significant difference between the two groups (both P > 0.05). Compensated blood loss, corresponding to transfusion, was noted significantly more in the active group compared to the stable group (P = 0.027). There was no significant difference with regard to functional recovery (P > 0.05). Conclusion: Active AS patients are at high risk for increased blood loss during THA compared to stable patients. The underlying mechanism includes disorders of the coagulation and fibrinolytic systems, poor nutrition status, osteoporosis, imbalance of oxidative-antioxidative status and local inflammatory reaction. It is strongly recommended to perform THA in AS patients with stable disease.

Circular RNAs (circRNAs) have emerged as important roles in various inflammatory processes of rheumatic diseases. However, their expression profiles and influences in the pathogenesis of ankylosing spondylitis (AS) remain unclear. In this study, we revealed the differential expression profiles of circRNAs in peripheral blood mononuclear cells (PBMCs) in AS by circRNA sequencing. We screened the differentially expressed circRNAs in AS and verified that hsa_circ_0000652 was upregulated and had potential to be a biomarker of progression. Functionally, hsa_circ_0000652 promoted proliferation and cytokine production in macrophages and inhibited apoptosis. Through dual-luciferase assays and RNA pull-down assays, we demonstrated that hsa_circ_0000652 acted as a competing endogenous RNA (ceRNA) by binding with hsa-miR-1179 and regulated OX40L, which is characterized as a co-stimulatory molecule and found to be upregulated in AS patients. As a result, hsa_circ_0000652 aggravated the inflammation in the coculture system containing CD4+ T cells and macrophages via OX40/OX40L interaction. Our findings suggest that hsa_circ_0000652 was upregulated in AS patients and may serve as a pro-inflammatory factor in macrophages and a positive regulator of OX40/OX40L by sponging hsa-miR-1179.

Background Many motion studies have shown that the inner bearing of bipolar prostheses moves less than expected under non-weight-bearing and static weight-bearing positions, which are not routine functional movements performed postoperatively. The aim of this study was to investigate the behaviours of bipolar prostheses during normal gait and simulative squatting. Methods Thirty-one femoral neck fracture patients were enrolled, and fluoroscopy examinations of walking on a treadmill, simulative squatting, and non-weight-bearing abduction-adduction and flexion-extension motions were performed at an average of 40 months postoperatively. The rate of acetabular cartilage degeneration was calculated. The ranges of motion of the outer bearing and inner bearing were determined, and the O/I ratios were calculated. Clinical efficacy was assessed by HHS and EQ-5D score. Results The inner bearing moved more than the outer bearing did, with an O/I ratio of 0.81, during the normal gait examination, while the motion of the outer bearing was obviously dominant during the simulative squatting and non-weight-bearing abduction-adduction and flexion-extension examinations. The mean acetabular cartilage degeneration rate was 0.82 ± 0.54 mm/year at the follow-up. In subgroup analyses, the motion of the outer bearing decreased to some extent with the increase in acetabular wear, and the corresponding O/I ratios among the groups showed a trend of decreasing first and then increasing. The HHS and EQ-5D scores of the patients with osteolysis and femoral stem loosening were much worse than those with fixed implants. Conclusion Bipolar prostheses do function as originally intended during gait, but movement primarily occurs at the outer bearing during other examinations. The motion patterns of bipolar prostheses change with the increase in acetabular wear.

Background: Growing evidence suggests that the pathogenesis of chronic obstructive pulmonary disease (COPD) is related to mitochondrial autophagy mediated by FUN14 domain protein 1 (FUNDC1). Recent studies have shown that puerarin has protective effects against excessive oxidative damage in cells. We hypothesized that puerarin might be involved in the progression of COPD induced by cigarette smoke extract (CSE) by regulating FUNDC1-mediated mitochondrial autophagy.Material/Methods: Different concentrations of puerarin were used to intervene in CSE-treated human bronchial epithelial cells (HBECs). MTT assay and flow cytometry were used to detect cell activity and apoptosis. The mitochondrial membrane potential (MMP) level, reactive oxygen species (ROS) content and ATP content were detected by flow cytometry or kits; Western Blotting was used to detect mitochondrial autophagy-related proteins expression such as DRP1, FUNDC1, PINK1, Parkin. Next, protein phosphatase inhibitor (PH0321) was used to inhibit the phosphorylation of FUNDC1, the changes of MMP, ROS, ATP and mitochondrial autophagy related proteins were detected. Furthermore, mitochondrial autophagy inhibitors (Mdivi) were used to block autophagy, and then the changes of mitochondrial autophagy, cell activity and apoptosis were detected, respectively. Finally, the changes of PI3K/AKT/mTOR signaling pathway-related proteins were detected by Western Blotting.Results: Puerarin reversed cell activity decrease and apoptosis increase of CSE-induced HBECs, and down-regulated apoptosis-related proteins expression. Puerarin up-regulated MMP level and ATP content in CSE-induced HBECs, and down-regulated ROS content and mitochondrial autophagy-related proteins expression. PH0321 promotes mitochondrial autophagy by promoting the dephosphorylation of FUNDC1, puerarin inhibits the dephosphorylation of FUNDC1, up-regulated the MMP level and ATP content of CSE-induced HBECs, reduces ROS content and mitochondrial autophagy-related proteins expression. Compared with Mdivi group, the protein expression changes of PINK1 and Parkin in puerarin-treated group were not significantly different, and the cell activity decrease and apoptosis increase of CSE-induced HBECs were also significantly reversed by puerarin, which was not significantly different from Mdivi group. Puerarin significantly upregulated the protein expression of p-PI3K, p-AKT and p-mTOR, suggesting that puerarin may participate in the progression of COPD by activating the PI3K/AKT/mTOR signaling pathway.Conclusions: Puerarin inhibits FUNDC1-mediated mitochondrial autophagy and CSE-induced apoptosis of HBECs by activating the PI3K/AKT/mTOR signaling pathway.

Background: Total hip arthroplasty (THA) has been highlighted as the best treatment option for ankylosing spondylitis (AS) patients with advanced hip involvement. The huge blood loss associated with THA is a common concern of postoperative complications. Disease activity is a specific reflection of systematic inflammation of AS. The purpose of this study was to determine the effect of disease activity on blood loss during THA in patients with AS. Methods: Forty-nine patients with AS who underwent unilateral THAs were retrospectively studied. Ankylosing Spondylitis Disease Activity Score (ASDAS) was employed to evaluate the disease activity. Orthopedic Surgery Transfusion Hemoglobin European Overview (OSTHEO) formula was used to assess the surgical blood loss. The patients were divided into active group (ASDAS≥1.3; n=32) and stable groups (ASDAS<1.3; n=17) based on the ASDAS. Peri-operative laboratory values, plain radiographs, intra-operative data, transfusion volume, and use of hemostatic agents were recorded and statistically analyzed. Results: The ASDAS, pre-operative C-reactive protein level, erythrocyte sedimentation rate, and fibrinogen concentration in the active group were higher than the stable group (all P <0.05); however, the pre-operative hemoglobin concentration and albumin level were higher in the stable group (both P <0.05). The total blood loss during THA in stable patients was 1415.31 mL and 2035.04 mL in active patients ( P =0.006). The difference between the two groups was shown to be consistent after excluding the gender difference ( P =0.030). A high transfusion rate existed in both groups (stable group, 76.47% with an average of 1.53 units; active group, 84.37% with an average of 2.31 units), but there was no significant difference between the two groups (both P >0.05). Compensated blood loss, corresponding to transfusion, was noted significantly more often in the active group compared to the stable group ( P =0.027). Conclusion: Active AS patients are at high risk for increased blood loss during THA compared to stable patients. The underlying mechanism includes disorders of the coagulation and fibrinolytic systems, poor nutrition status, osteoporosis, imbalance of oxidative–antioxidative status and local inflammatory reaction. It is strongly recommended to perform THA in AS patients with stable disease.

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