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The purpose of this study was to compare the clinical outcomes of impacted bone graft with or without recombinant human bone morphogenetic protein-2 (rhBMP-2) for osteonecrosis of the femoral head (ONFH). We examined the effect of bone-grafting through a window at the femoral head-neck junction, known as the “light bulb” approach, for the treatment of ONFH with a combination of artificial bone (Novobone) mixed with or without rhBMP-2. A total of 42 patients (72 hips) were followed-up from 5 to 7.67 years (average of 6.1 years). The patients with and without BMP were the first group (IBG+rhBMP-2) and the second group (IBG), respectively. The clinical effectiveness was evaluated by Harris hip score (HHS). The radiographic follow-up was evaluated by pre-and postoperative X-ray and CT scan. Excellent, good, and fair functions were obtained in 36, 12, and 7 hips, respectively. The survival rate was 81.8% and 71.8% in the first and second group, respectively. However, the survival rate was 90.3% in ARCO stage IIb, c, and only 34.6% in ARCO stage IIIa(P<0.05). It was concluded that good and excellent mid-term follow-up could be achieved in selected patients with ONFH treated with impacted bone graft operation. The rhBMP-2 might improve the clinical efficacy and quality of bone repair.

The SVM method achieved excellent performance as measured by the Matthews correlation coefficient (MCC = 0.45) using a 7-fold cross validation on a database of 426 non-homologous protein chains. To our best knowledge, this MCC value is the highest achieved so far for predicting beta-turn. The overall prediction accuracy Qtotal was 77.3%, which is the best among the existing prediction methods. Among its unique attractive features, the present SVM method avoids overtraining and compresses information and provides a predicted reliability index.

Our results prompt another mechanism of anti-fibrotic renal protection of renalase, which may be partly associated with inhibiting oxidative stress. These data provided another theoretical basis that supplementation with exogenous renalase may be a promising strategy for slowing or halting the progression of CKD.

Background:Controversies about the rational positioning of the tibial component in unicompartmental knee arthroplasty (UKA) still exist. Previous finite element (FE) studies were rare, and the results varied. This FE study aimed to analyze the influence of the tibial component coronal alignment on knee biomechanics in mobile-bearing UKA and find a ration range of inclination angles.Methods:A three-dimensional FE model of the intact knee was constructed from image data of one normal subject. A 1000 N compressive load was applied to the intact knee model for validating. Then a set of eleven UKA FE models was developed with the coronal inclination angles of the tibial tray ranging from 10° valgus to 10° varus. Tibial bone stresses and strains, contact pressures and load distribution in all UKA models were calculated and analyzed under the unified loading and boundary conditions.Results:Load distribution, contact pressures, and contact areas in intact knee model were validated. In UKA models, von Mises stress and compressive strain at proximal medial cortical bone increased significantly as the tibial tray was in valgus inclination >4°, which may increase the risk of residual pain. Compressive strains at tibial keel slot were above the high threshold with varus inclination >4°, which may result in greater risk of component migration. Tibial bone resection corner acted as a strain-raiser regardless of the inclination angles. Compressive strains at the resected surface slightly changed with the varying inclinations and were not supposed to induce bone resorption and component loosening. Contact pressures and load percentage in lateral compartment increased with the more varus inclination, which may lead to osteoarthritis progression.Conclusions:Static knee biomechanics after UKA can be greatly affected by tibial component coronal alignment. A range from 4° valgus to 4° varus inclination of tibial component can be recommended in mobile-bearing UKA.

BackgroundThe minimally invasive Oxford unicompartmental knee arthroplasty (UKA) is a demanding procedure but has many advantages compared with total knee arthroplasty (TKA). The aim of this observational study was to investigate the learning curve of one experienced surgeon introducing minimally invasive Oxford phase 3 UKA into his routine clinical practice.MethodsThe first 50 consecutive cases of minimally invasive Oxford phase 3 UKA performed by one surgeon were evaluated to determine whether there was an association between outcomes and the cumulative number of cases performed, indicating the presence of learning curve. The cohort was divided into two groups: group A comprised the first 25 cases and group B cases 26–50. Duration of surgery, blood loss, Hospital for Special Surgery score, range of motion, complications, and the radiographical position of the implant were compared between the groups. The cumulative summation test for learning curve (LC-CUSUM) was then used to further analyze the learning curve.ResultsThe mean age and follow-up were 64.4 years and 50.9 months, respectively. The duration of surgery and blood loss were significantly more favorable in group B. The length of incision gradually reduced from 9.7 ± 1.3 to 8.5 ± 1.1 cm. Failures were identified in nine patients (18%). Two revisions and two dislocations were encountered in group A; one revision was performed 4 years after surgery for a patient in group B because of a fracture. One case of lateral compartment osteoarthritis was identified in group A. Two patients in each group reported continuing unexplained pains. CUSUM analysis showed that failure rates diminished rapidly after 16 cases and reached an acceptable rate after 29 cases.ConclusionsMinimally invasive Oxford phase 3 UKA for anteromedial osteoarthritis is a demanding procedure, but satisfactory outcomes can be achieved after approximately 25 cases.

Renal interstitial fibrosis is a common pathway for the progression of chronic kidney disease (CKD) to end-stage renal disease. Renalase, acting as a signaling molecule, has been reported to have cardiovascular and renal protective effects. However, its role in renal fibrosis remains unknown. In this study, we evaluated the therapeutic efficacy of renalase in rats with complete unilateral ureteral obstruction (UUO) and examined the inhibitory effects of renalase on transforming growth factor-β1 (TGF-β1)-induced epithelial–mesenchymal transition (EMT) in human proximal renal tubular epithelial (HK-2) cells. We found that in the UUO model, the expression of renalase was markedly downregulated and adenoviral-mediated expression of renalase significantly attenuated renal interstitial fibrosis, as evidenced by the maintenance of E-cadherin expression and suppressed expression of α-smooth muscle actin (α-SMA), fibronectin and collagen-I. In vitro, renalase inhibited TGF-β1-mediated upregulation of α-SMA and downregulation of E-cadherin. Increased levels of Phospho-extracellular regulated protein kinases (p-ERK1/2) in TGF-β1-stimulated cells were reversed by renalase cotreatment. When ERK1 was overexpressed, the inhibition of TGF-β1-induced EMT and fibrosis mediated by renalase was attenuated. Our study provides the first evidence that renalase can ameliorate renal interstitial fibrosis by suppression of tubular EMT through inhibition of the ERK pathway. These results suggest that renalase has potential renoprotective effects in renal interstitial fibrosis and may be an effective agent for slowing CKD progression.

Epithelial-mesenchymal transition (EMT) of tubular epithelial cells is a key event in renal interstitial fibrosis and the progression of chronic kidney disease (CKD). Apelin is a regulatory peptide involved in the regulation of normal renal hemodynamics and tubular functions, but its role in renal fibrosis remains unknown. In this study, we examined the inhibitory effects of apelin on transforming growth factor-β1 (TGF-β1)-induced EMT in HK-2 cells, and evaluated its therapeutic efficacy in mice with complete unilateral ureteral obstruction (UUO). In vitro, apelin inhibited TGF-β1-mediated upregulation of α-smooth muscle actin (α-SMA) and downregulation of E-cadherin. Increased levels of phosphorylated Smad-2/3 and decreased levels of Smad7 in TGF-β1-stimulated cells were reversed by apelin co-treatment. In the UUO model, administration of apelin significantly attenuated renal interstitial fibrosis, as evidenced by the maintenance of E-cadherin and laminin expression, and markedly suppressed expression of α-SMA, TGF-β1 and its type I receptor, as well as interstitial matrix components. Interestingly, in UUO mice, there was a reduction in the plasma level of apelin, which was compensated by upregulation of APJ expression in the injured kidney. Exogenous supplementation of apelin normalized the level of plasmatic apelin and renal APJ. In conclusion, our study provides the first evidence that apelin is able to ameliorate renal interstitial fibrosis by suppression of tubular EMT through a Smad-dependent mechanism. The apelinergic system itself may promote some compensatory response in the renal fibrotic process. These results suggest that apelin has potential renoprotective effects and may be an effective agent for retarding CKD progression.