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Serum uric acid (SUA) is involved in the development of cardiovascular disease (CVD). However, information on the dose-response relationship between SUA and CVD is limited in the Chinese population. This study aimed to investigate the potential nonlinear dose-response association of SUA with CVD risk in a Chinese population and to explore the effect of sex on these associations. Cross-sectional data, from 6252 Chinese adults aged 30–74 years who participated in the China Health and Nutrition Survey 2009, were stratified by SUA deciles. The 10-year risk of CVD was determined using the Framingham risk score. A restricted cubic spline (RCS) was incorporated into the logistic models to assess the nonlinear relationship between SUA and CVD. Among the participants, 65%, 20%, and 15% had low, moderate, and high 10-year CVD risks, respectively. Compared with the reference SUA strata of 225 to <249 μmol/L, CVD risk was significantly increased at SUA ≥294 μmol/L, with adjusted ORs ranging from 2.39 (1.33–4.33) to 4.25 (2.37–7.65). An increasingly higher nonsignificant CVD risk was found at SUA <225 μmol/L and showed a nonlinear U-shaped association. In the fitted RCS model, an approximate U-shaped association between SUA and CVD risk scores was found in women, but this significant nonlinear relationship was not found in men. This study showed that both lower and higher SUA levels were associated with a higher 10-year CVD risk among Chinese adults, forming a U-shaped relationship, and this pattern was particularly pronounced for women. • In this nationally population-based study, both lower and higher SUA levels were associated with an increased CVD risk. • A U-shaped association pattern for 10-year CVD risk and SUA levels was found. • This U-shaped pattern was particularly pronounced for women, with the lowest CVD risk score at the SUA level of 250 µmol/L. • However, this significant nonlinear relationship was not found in men. [ABSTRACT FROM AUTHOR]

Background: Osteonecrosis of the femoral head (ONFH) often affects young, active adults and leads to the destruction of the hip joint and disabling arthritis. Several procedures have been developed to prevent conversion to total hip arthroplasty (THA), especially in young patients who have a high rate of hip revision surgery. The aim of this long-term follow-up is to analyze the results of vascularized iliac bone flap transfer for ONFH treatment.Methods: We retrospectively reviewed 856 patients (1006 hips) who accepted hip-preserving surgery with vascularized iliac bone grafting due to ONFH (Ficat and Arlet stages II-IV) from January 1985 to December 2012 at our hospital. Radiographic assessment was performed with the Ficat and Arlet system, clinical assessment was performed with the Harris Hip Score system, and quality of life was evaluated with the 36-Item Short Form Survey. The hips included 575 stage II hips, 382 stage III hips, and 49 stage IV hips. We defined clinical failure as conversion to THA or any other hip-preserving surgery because of hip symptoms.Results: A total of 856 patients (1006 hips) were eventually followed up with an average time of 15 years (range 5-25). In total, 75 patients were lost to follow-up, and 105 hips were converted to THA. The average Harris Hip Score was 87.43 ± 6.42 points at the last follow-up, representing a great improvement compared to the 66.42 ± 6.52 points obtained preoperatively. The Kaplan-Meier survival analysis showed no difference in the 15-year survival rate between patients with stages II and III disease (using THA as an end point). However, the survival rate was lower for patients with stage IV disease than that for patients with stages II and III disease. The survival rate for patients in the glucocorticoid group was lower than that for patients in the idiopathic, alcoholic, and trauma groups. The Physical Component Summary scores ranged from 78 ± 10 to 85 ± 14 postoperatively compared to 30 ± 14 to 55 ± 15 preoperatively, and the postoperative Mental Component Summary scores (range from 34 ± 11 to 59 ± 12) were significantly higher than the preoperative scores (range from 72 ± 11 to 90 ± 10), representing great improvement in patient quality of life. Postoperative complications occurred in 86 patients (4.5%) during the follow-up, including 23 patients with deep venous thrombosis, 16 patients with meralgia paresthetica (which resolved), and 47 patients with secondary wound healing.Conclusion: The vascularized iliac bone flap grafting technique yields significant improvement (particularly in the precollapse disease stages in young patients) for restoration of the biomechanical support of the collapsed femoral head and reconstruction of the blood supply to the osteonecrotic area. This procedure allows these patients to avoid or delay the need for THA surgery. [ABSTRACT FROM AUTHOR]

Mg-based alloys, as the potential orthopaedic implant, can self-degrade to avoid second operation for its remove, and enable to promote bone repair; however, the underlying molecular mechanisms remain unclear. In the present study, we examined the effect of Mg ions on osteogenesis, chemotaxis and anti-alkaline stress in hFOB1.19 human osteoblast cells to simulate bone-repairing effect of a biodegradable Mg-based alloy implant in vitro , and explored the regulatory role of the transient receptor potential melastatin 7 (TRPM7)/phosphoinositide 3-kinase (PI3K) signalling pathway in the process of Mg ion-induced bone repair by knockdown of TRPM7 and antagonizing PI3K activity. Results indicate that Mg ions up-regulated the expression of Runx2 and alkaline phosphatase (ALP) through TRPM7/PI3K signalling pathway, which could significantly enhance the osteogenic activity of human osteoblasts. Furthermore, the expression levels of MMP2, MMP9 and vascular endothelial growth factor (VEGF) were increased by TRPM7/PI3K signalling pathway, which recruits osteoblasts from low- to high-Mg ion environments by inducing cell migration. Although an alkaline environment has antibacterial effects, alkaline stress can cause cytotoxicity and induce cell death. Finally, we found that Mg ions could activate PI3K phosphorylation to promote cell growth and survival, protecting cells against the alkaline-stress-induced cytotoxicity caused by the degradation of Mg-based alloy implants. Our study not only revealed the molecular mechanism of Mg in promoting bone repair but also explained the protective effects of Mg ions on osteoblasts in an alkaline environment, which provides a theoretical basis and new directions for the application of Mg-based alloy implant material in orthopaedics fixations and osteosarcoma treatment. Statements of Significance As a potential biomaterial for orthopaedic implant, biodegradable magnesium has several advantages including self-degradation and bone repair promotion; however, the underlying mechanisms and effective concentration by which molecular regulates the bone repair remain unclear. The present study revealed that Mg ion and its effective concentration for activating PI3K phosphorylation via TRPM7, which causes three processes affecting bone repair, namely, osteoblast recruitment, osteogenesis and resistance to alkaline stress in human osteoblast. Therefore, our results have provided insight into the underlying molecular biological basis, and guidance for manipulating degradation rate, such as surface modification, of orthopaedic Mg-based implants. [ABSTRACT FROM AUTHOR]