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Aseptic loosening (AL), secondary to particle-caused periprosthetic osteolysis, is one of the main reasons of artificial joint failure. Suppressing the macrophage inflammatory response caused by wear particles extends the life of prosthesis, and the long noncoding RNAs (lncRNAs) may play a predominant part in it. Here, titanium particles' (TiPs') stimulation increases both the cytoplasmic and nuclear levels of lncRNA Neat1 in bone marrow derived macrophages (BMDMs), which further induces the inflammatory response. Mechanically, Neat1 facilitates Bruton's tyrosine kinase (BTK) transcription by reducing the transcriptional factor KLF4, which further activates the NF-κB pathway, NLRP3 inflammation, and M1 polarization in BMDMs. Cytoplasmic Neat1 also works as an miRNA sponge in miR-188-5p-regulated BTK expression in the post-transcriptional stage. In vivo, Neat1 downregulation can reduce the TiP-induced pro-inflammatory factors and reverse the osteolysis induced by BTK overexpression. In addition, the PLGA-based microparticles loaded with si-Neat1 are developed for the treatment of the mouse calvarial osteolysis model via local injection, presenting satisfactory anti-osteolysis efficacy. These findings indicate that Neat1 is a key regulator of AL. STATEMENT OF SIGNIFICANCE: Due to released particles, aseptic loosening (AL) is the most common reason for prosthesis failure and surgical revision and represents a substantial economic burden worldwide. Herein, we reported that lncRNA Neat1 is a key regulator in regulating wear particles-induced osteolysis by activating NF-κB pathway, NLRP3 inflammation and M1 polarization via BTK, and the underlying mechanisms of Neat1-BTK interaction were further portrayed. For potential clinical application, the microparticles are developed for effective si-Neat1 delivery, leading to a dramatically enhanced effect for the treatment of osteolysis, which might be a novel strategy to extend the life of the implant.

Increasing evidence shows that adipokines play a vital role in the development of rheumatoid arthritis (RA). Fatty acid-binding protein 4 (FABP4), a novel adipokine that regulates inflammation and angiogenesis, has been extensively studied in a variety of organs and diseases. However, the effect of FABP4 on RA remains unclear. Here, we found that FABP4 expression was upregulated in synovial M1-polarized macrophages in RA. The increase in FABP4 promoted synovitis, angiogenesis, and cartilage degradation to exacerbate RA progression in vivo and in vitro, whereas BMS309403 (a FABP4 inhibitor) and anagliptin (dipeptidyl peptidase 4 inhibitor) inhibited FABP4 expression in serum and synovial M1-polarized macrophages in mice to alleviate RA progression. Further studies showed that constitutive activation of mammalian target of rapamycin complex 1 (mTORC1) by TSC1 deletion specifically in the myeloid lineage regulated FABP4 expression in macrophages to exacerbate RA progression in mice. In contrast, inhibition of mTORC1 by ras homolog enriched in brain (Rheb1) disruption specifically in the myeloid lineage reduced FABP4 expression in macrophages to attenuate RA development in mice. Our findings established an essential role of FABP4 that is secreted by M1-polarized macrophages in synovitis, angiogenesis, and cartilage degradation in RA. BMS309403 and anagliptin inhibited FABP4 expression in synovial M1-polarized macrophages to alleviate RA development. Hence, FABP4 may represent a potential target for RA therapy.

SUMMARYOver the past few decades, seismic studies have revealed complex structural anomalies in the Earth’s deep interior at various scales, such as large low-shear-velocity provinces (LLSVPs) and ultra-low velocity zones (ULVZs) in the lowermost mantle, and small-scale scatterers in the mid-mantle. These structures which are critical for better understanding of the geodynamics and evolution of the deep Earth, need to be further resolved by high-resolution imaging techniques. The spectral-element method (SEM) can be used to accurately simulate seismic wave propagation in heterogeneous Earth models, and its application in full-waveform inversion (FWI) provides a promising high-resolution and high-fidelity imaging technique. But it can be computationally prohibitive when used to model small scale structures in the deep Earth based upon high-frequency seismic waves. The heavy computational cost can be circumvented by using hybrid methods, which restrict the main computation by SEM solver to only a small target region (e.g. above the CMB) encompassing possible 2-D/3-D anomalies, and apply efficient analytical or numerical methods to calculate the wavefield for 1-D background models. These forward modelling tools based on hybrid methods can be then used in the so-called ‘box tomography’ approach to resolve fine-structures in the deep Earth.In this study, we outline the theory of a hybrid method used to model small scale structures in the deep Earth and present its implementation based on SEM solvers in a three-step workflow. First, the wavefield generated by the source is computed for the 1-D background model with traction and velocity saved for the virtual boundary of the target region, which are then used as boundary inputs to simulate the wavefield in the target region based on absorbing boundary condition in SEM. In the final step, the total wavefield at receivers is reconstructed based upon the total wavefield on the virtual boundary computed in the previous step. As a proof-of-concept study, we demonstrate the workflow of the hybrid method based on a 2-D SEM solver. Examples of the hybrid method applied to a coupled fluid–solid model show that our workflow can accurately recover the scattered waves back to the surface. Furthermore, we benchmark the hybrid method on a realistic heterogeneous Earth model built from AK135-F and show how teleseismic scattered waves can be used to model deep Earth structures. By documenting the theory and SEM implementation of the hybrid method, our study lays the foundation for future two-way coupling of 3-D SEM solver with other efficient analytic or numerical 1-D solvers.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovitis. Synovitis can cause joint injury by releasing inflammatory factors and metalloproteinases (MMPs). Therefore, it is necessary to find drugs that can control synovitis in the process of RA. Herein, we investigate the anti-inflammatory effect of Hesperidin (HSN) on fibroblast-like synovial (FLS) cells induced by lipopolysaccharide (LPS) and the protective action of M1 polarization level of synovial macrophages on antigen-induced arthritis (AIA) in order to elucidate the reduction of inflammatory cytokines and MMPs and the inhibition of macrophage activation. The functional effect of HSN on LPS-induced mRNA and protein expressions of inflammatory cytokines and MMPs in FLS cells as well as on LPS-induced macrophage M1 and M2 polarization markers was determined by quantitative real-time PCR (qPCR) or Western blot analyses, respectively. AIA in 2-month-old mice was generated using intraperitoneal injection with HSN (20 mg/kg/day) or LY294002 (20 mg/kg/day). The results show HSN significantly inhibited the LPS-induced gene expression of the inflammatory mediators. Furthermore, treatment with HSN relieved the antigen-induced arthritis and reduced the protein levels of MMP3, MMP9, and MMP13 in FLS and inhibited the polarization of macrophages to M1. Based on the results of our analyses, we concluded that HSN has significant anti-inflammatory activities and reduces the potential of MMPs in rheumatoid arthritis and the degree of polarization of macrophages to M1. Through the study of signaling pathways, we established that the inhibition of the PI3K/AKT signaling pathway by HSN may show therapeutic effects in the progression of rheumatoid arthritis.

Increasing evidences show that aberrant subchondral bone remodeling plays an important role in the development of osteoarthritis (OA). However, how subchondral bone formation is activated and the mechanism by which increased subchondral bone turnover promotes cartilage degeneration during OA remains unclear. Here, we show that the mechanistic target of rapamycin complex 1 (mTORC1) pathway is activated in subchondral bone preosteoblasts (Osterix+) from OA patients and mice. Constitutive activation of mTORC1 in preosteoblasts by deletion of the mTORC1 upstream inhibitor, tuberous sclerosis 1, induced aberrant subchondral bone formation, and sclerosis with little-to-no effects on articular cartilage integrity, but accelerated post-traumatic OA development in mice. In contrast, inhibition of mTORC1 in preosteoblasts by disruption of Raptor (mTORC1-specific component) reduced subchondral bone formation and cartilage degeneration, and attenuated post-traumatic OA in mice. Mechanistically, mTORC1 activation promoted preosteoblast expansion and Cxcl12 secretion, which induced subchondral bone remodeling and cartilage degeneration during OA. A Cxcl12-neutralizing antibody reduced cartilage degeneration and alleviated OA in mice. Altogether, these findings demonstrate that mTORC1 activation in subchondral preosteoblasts is not sufficient to induce OA, but can induce aberrant subchondral bone formation and secrete of Cxcl12 to accelerate disease progression following surgical destabilization of the joint. Pharmaceutical inhibition of the pathway presents a promising therapeutic approach for OA treatment.

Objectives The role of mechanical stress and transforming growth factor beta 1 (TGF-β1) is important in the initiation and progression of osteoarthritis (OA). However, the underlying molecular mechanisms are not clearly known. Methods In this study, TGF-β1 from osteoclasts and knee joints were analyzed using a co-cultured cell model and an OA rat model, respectively. Five patients with a femoral neck fracture (four female and one male, mean 73.4 years (68 to 79)) were recruited between January 2015 and December 2015. Results showed that TGF-β1 was significantly upregulated in osteoclasts by cyclic loading in a time- and dose-dependent mode. The osteoclasts were subjected to cyclic loading before being co-cultured with chondrocytes for 24 hours. Results A significant decrease in the survival rate of co-cultured chondrocytes was found. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) assay demonstrated that mechanical stress-induced apoptosis occurred significantly in co-cultured chondrocytes but administration of the TGF-β1 receptor inhibitor, SB-505124, can significantly reverse these effects. Abdominal administration of SB-505124 can attenuate markedly articular cartilage degradation in OA rats. Conclusion Mechanical stress-induced overexpression of TGF-β1 from osteoclasts is responsible for chondrocyte apoptosis and cartilage degeneration in OA. Administration of a TGF-β1 inhibitor can inhibit articular cartilage degradation. Cite this article: R-K. Zhang, G-W. Li, C. Zeng, C-X. Lin, L-S. Huang, G-X. Huang, C. Zhao, S-Y. Feng, H. Fang. Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1). Bone Joint Res 2018;7:587–594. DOI: 10.1302/2046-3758.711.BJR-2018-0057.R1.

The BESIII experiment has collected $e^+e^-$ collision data samples corresponding to integrated luminosities of $2.93~\rm{fb^{-1}}$ and $3.19~\rm{fb^{-1}}$ at center-of-mass energies of $3.773~\rm{GeV}$ and $4.178~\rm{GeV}$, respectively. We report the measurements of strong phase differences in $D^{0}$ decays, including $K_{S/L}\pi^{+}\pi^{-}$ and $K_{S/L}K^{+}K^{-}$, which can reduce the systematic uncertainty of $\gamma/\phi_{3}$ measurement at LHCb and Belle II. In addition, we report the amplitude analyses and the measurements of the absolute branching fractions of $D^{+}$, $D^{0}$, and $D_{s}$ decays.

We report on an analysis of the decay J/ψ→γπ0η′ using a sample of (1310.6±7.0)×106J/ψ events collected with the BESIII detector. We search for the CP-violating process ηc→π0η′ and a dark gauge boso ...

MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR‐497, leucine‐rich alpha‐2‐glycoprotein‐1 (LRG1) and transforming growth factor beta 1 (TGF‐β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR‐497/LRG1/TGF‐β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR‐497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR‐497 or depleted LRG1 for further verification. MiR‐497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF‐β1/Smads signalling pathway‐related factors were detected. MiR‐497 was poorly expressed while LRG1 was highly expressed and TGF‐β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR‐497 up‐regulation or LRG1 down‐regulation activated TGF‐β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR‐497 restoration or LRG1 knockdown activated TGF‐β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR‐497 up‐regulation or LRG1 down‐regulation promotes osteoblast viability and collagen synthesis via activating TGF‐β1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment.

Spinal cord injury (SCI) is lead to locomotor impairment because of neurological damage after following trauma. Quercetin (Que) has been confirmed to have a neuro-protective effect during nerve damage processes. The purpose of this study was to determine the roles of Que in functional recovery, cavity formation, astrocyte activation, and nerve regeneration following SCI. Sprague-Dawley rats were randomly divided into three groups: Sham group, SCI group, and Que + SCI group. A rat model of SCI was made at T10 using the modified Allen's method. In the Que + SCI group, animals underwent laminectomy and were then intraperitoneally injected with 20 mg/kg Que for 7 days. Locomotor function was determined with the Basso, Beattie, Bresnahan (BBB) scores at 1, 3, 5, and 7 days post-injury. At 7 days post-injury, somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) were recorded. Hematoxylin-Eosin (HE) staining was used to investigate cavity formation. Astrocyte activation was assayed by immunohistochemistry staining with an antibody specific for glial fibrillary acidic protein (GFAP), as well as the expression of GFAP and S100β. Axons were stained using an antibody specific for neurofilament 200 (NF200) and 5-hydroxytryptamine (5-HT). In addition, the protein level of BDNF, p-JNK2, and p-STAT3 was detected using Western blot. Que promoted locomotor function and electrophysiological recovery, reduced cavity formation, contributed to astrocyte activation and axonal regeneration after acute SCI. Moreover, Que up-regulated the expression of BDNF, but reduced p-JNK2 and p-STAT3 expression after acute SCI. Taken together, Que promoted locomotor and electrophysiological functional recovery, astrocyte activation and axonal regeneration after acute SCI, possibly through BDNF and JAK2/STAT3 signaling pathways.

Sonic log records, including measurements of wave speeds in boreholes, provide critical input to the geological, geophysical, and petrophysical studies of a region under exploration. 1D background models are routinely built based on sonic log records for applications such as seismic imaging of hydrocarbon reservoirs and microseismic source inversions. Smoothing or ‘upscaling’ techniques are required to produce models in coarser scales than the very fine layers in the raw log data. In this paper, we follow the recently popular homogenization theory, derive its application to the special case of 1D TI models for both P-SV and SH waves, and show that it is consistent with the Backus averaging technique commonly used to upscale 1D fine-layered models. We examine a study case of sonic log data from a well in the Horn River Basin in northeastern British Columbia, a region known for its tight shale-gas deposit. We demonstrate the computational accuracy and efficiency gained by proper upscaling procedures for spectral-element simulations of seismic wave propagation, and discuss the effect of control parameters on wavefield recovery.

BACKGROUND Surgical treatment of acetabular fractures is one of the greatest challenges for orthopedic surgeons. Fixation of most displaced fractures requires extensive exposure, which may lead to complications, including blood loss, neural or vascular injury, postoperative infection, wound healing problems, and heterotopic bone formation. MATERIAL AND METHODS This study was conducted to certify an anatomic plate with an anterior column lag screw guiding device to repair the posterior acetabulum. Complete pelvic spiral computed tomography (CT) scan data were collected from 56 patients. The posterior column of the acetabulum was simulated with a lag screw. The guiding device for the plate was designed by measuring the position of the screw point and the direction and maximum diameter of the screw. RESULTS The distance from the screw point to the apex of the greater sciatic notch was farther in women than in men. The distance from the screw point to the ischial spine was also farther in women than in men. The q angle (front inclination angle) of the screw was lower in women than in men. The j angle (camber screw angle) was greater in women than in men. The success rate when using the guided device was significantly higher than when using traditional pedicle screws. CONCLUSIONS The guided device was very useful for improving placement success and accuracy rates of the acetabular posterior anatomical anterior column plate using antegrade lag screws, and for reducing surgical risk and injury.

Background The aim of this study was to provide valid data for a plate-screw fixation model for fractured posterior-anterior columns of the acetabulum. Material/Methods Nineteen cadaveric bony hemi-pelvis specimens were obtained and 50 healthy adults were enrolled. The modified Stoppa approach and computed tomography (CT) imaging were used to collect the measured parameter data of the module. Results The measured parameter data were as follows: OP, 0.96±0.32 cm in females and 0.92±0.16 cm in males (P>0.05); PI, 0.98±0.28 cm in females, and 0.75±0.23 cm in males (P>0.05); ∠θ, 59.68°±6.28° in females and 56.75°±3.22° in males (P>0.05); and ∠ϕ, 41.27°±2.76° in females and 34.31°±2.78° in males (P0.05); OP, 1.06±0.29 cm in females and 1.12±0.24 cm in males (P>0.05); ∠θ, 55.33°±4.00° in females and 55. 50°±3.43° in males (P>0.05); and ∠ϕ was 39.21°±2.45°in females and 35.58°±2.31°in males (P0.05). Conclusions The measured parameter data obtained in healthy adults and cadaveric specimens provided an anatomic basis for the designation of the guide module, and thus confirmed the accuracy and safety of screw placement in fractured columns of the acetabulum.

Inflammation and oxidative stress have been reported to play critical roles in the pathogenesis of neurodegenerative disease. Forsythiaside A, a phenylethanoside product isolated from air-dried fruits of Forsythia suspensa, has been reported to have anti-inflammatory and antioxidant effects. In this study, the anti-inflammatory effects of forsythiaside A on LPS-stimulated BV2 microglia cells and primary microglia cells were investigated. The production of inflammatory mediators TNF-α, IL-1β, NO and PGE2 were detected in this study. NF-κB, nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) expression were detected by western blot analysis. Our results showed that forsythiaside A significantly inhibited LPS-induced inflammatory mediators TNF-α, IL-1β, NO and PGE2 production. LPS-induced NF-κB activation was suppressed by forsythiaside A. Furthermore, forsythiaside A was found to up-regulate the expression of Nrf2 and HO-1. In conclusion, this study demonstrates that forsythiaside A inhibits LPS-induced inflammatory responses in BV2 microglia cells and primary microglia cells through inhibition of NF-κB activation and activation of Nrf2/HO-1 signaling pathway.

ObjectivesTo investigate the roles and regulatory mechanisms of synovial macrophages and their polarisation in the development of osteoarthritis (OA).MethodsSynovial tissues from normal patients and patients with OA were collected. M1 or M2-polarised macrophages in synovial tissues of patients with OA and OA mice were analysed by immunofluorescence and immunohistochemical staining. Mice with tuberous sclerosis complex 1 (TSC1) or Rheb deletion specifically in the myeloid lineage were generated and subjected to intra-articular injection of collagenase (collagenase-induced osteoarthritis, CIOA) and destabilisation of the medial meniscus (DMM) surgery to induce OA. Cartilage damage and osteophyte size were measured by Osteoarthritis Research Society International score and micro-CT, respectively. mRNA sequencing was performed in M1 and control macrophages. Mice and ATDC5 cells were treated with R-spondin-2 (Rspo2) or anti-Rspo2 to investigate the role of Rspo2 in OA.ResultsM1 but not M2-polarised macrophages accumulated in human and mouse OA synovial tissue. TSC1 deletion in the myeloid lineage constitutively activated mechanistic target of rapamycin complex 1 (mTORC1), increased M1 polarisation in synovial macrophages and exacerbated experimental OA in both CIOA and DMM models, while Rheb deletion inhibited mTORC1, enhanced M2 polarisation and alleviated CIOA in mice. The results show that promoting the macrophage M1 polarisation leads to exacerbation of experimental OA partially through secretion of Rspo2 and activation of β-catenin signalling in chondrocytes.ConclusionsSynovial macrophage M1 polarisation exacerbates experimental CIOA partially through Rspo2. M1 macrophages and Rspo2 are potential therapeutic targets for OA treatment.

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The roles of different immune cell populations and cytokines in bone metabolism have been extensively investigated. However, the influence of whole immune organ removal on osteopathology remains unknown. In the current study, we investigated the effects of splenectomy on bone metabolism and microarchitecture in rats with or without concurrent ovariectomy. Ovariectomized (OVX) rats were used as osteoporosis model. Sixty 12-week-old female rats were randomized into 4 groups (n = 15): sham, splenectomized (SP), ovariectomized, as well as ovariectomized and splenectomized (OVX + SP). Bone microarchitecture was assessed by micro CT analysis at 4 week and 12 week post-operation, respectively. Bone pathology and metabolism were evaluated via immunohistochemical staining. The serum levels of alkaline phosphatase (ALP), tumor necrosis factor-alpha (TNF-α), tartrate-resistant acid phosphatase 5b (Tracp5b), and C-terminal telopeptide (CTx) were analyzed at 4 and 12 weeks post-operation. Removal of the spleen led to alterations in the homeostasis of bone metabolism and increased bone formation in rats. In this study, our findings indicate that the spleen is involved in skeletal metabolism. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1356–1363, 2015.

PI3K/AKT signaling is essential in regulating pathophysiology of osteoarthritis (OA). However, its potential modulatory role in early OA progression has not been investigated yet. Here, a mouse destabilization OA model in the tibia was used to investigate roles of PI3K/AKT signaling in the early subchondral bone changes and OA pathological process. We revealed a significant increase in PI3K/AKT signaling activation which was associated with aberrant bone formation in tibial subchondral bone following destabilizing the medial meniscus (DMM), which was effectively prevented by treatment with PI3K/AKT signaling inhibitor LY294002. PI3K/AKT signaling inhibition attenuated articular cartilage degeneration. Serum and bone biochemical analyses revealed increased levels of MMP-13, which was found expressed mainly by osteoblastic cells in subchondral bone. However, this MMP-13 induction was attenuated by LY294002 treatment. Furthermore, PI3K/AKT signaling was found to enhance preosteoblast proliferation, differentiation, and expression of MMP-13 by activating NF-B pathway. In conclusion, inhibition of PI3K/AKT/NF-B axis was able to prevent aberrant bone formation and attenuate cartilage degeneration in OA mice. Refereed/Peer-reviewed

Objective This study was to compare the effectiveness of Masquelet technique versus Ilizarov bone transport in the treatment of lower extremity bone defects following posttraumatic osteomyelitis. Patients and methods We retrospectively reviewed 39 patients who had been treated at our department for lower extremity bone defects following posttraumatic osteomyelitis. They were 30 males and 9 females with a mean age of 39.18 (range, 12–63 years). The infected bone defects involved 26 tibias and 13 femurs. The mean length of the bone defects after radical debridement was 6.76 cm (range, 2.7–15.7 cm). Masquelet technique (MT, group A) was used in 20 patients and Ilizarov bone transport (IBT, group B) in 19 ones. The measurements were bone outcomes (union, deformity, infection and leg-length discrepancy) and functional outcomes (significant limping, joint contracture, soft tissue dystrophy, pain and inactivity). Results The mean follow-up after removal of the apparatus was 25.26 months (range, 14–51 months). The mean finite fixator time was 10.15 months (range, 8–14 months) in group A versus 17.21 months (range, 11–24 months) in group B. The bone outcomes were similar between groups A and B [excellent (5 vs. 7), good (10 vs.9), fair (4 vs. 2) and poor (1 vs. 1)]; group A showed better functional outcomes than group B [excellent (8 vs. 3), good (9 vs. 6), fair (3 vs. 8) and poor (0 vs. 2)]. Conclusions In the treatment of segmental lower extremity bone defects following posttraumatic osteomyelitis, both IBT and MT can lead to satisfactory bone results while MT had better functional results, especially in femoral cases. IBT should be preferred in cases of limb deformity and MT may be a better choice in cases of periarticular bone defects.

Objective Myostatin, a member of the transforming growth factor-β family, contributes to joint deterioration in mice. Thus, we aimed to assess the correlation of myostatin concentrations with the presence and severity of knee osteoarthritis (OA). Material and Methods We determined serum and synovial fluid (SF) myostatin concentrations in a population of 184 patients with knee OA and 109 healthy controls. Results The knee OA group presented with higher serum myostatin concentrations than the controls. Knee OA patients with KL grade 4 showed higher serum and SF myostatin concentrations compared with those with KL grade 2 and 3. Knee OA patients with KL grade 3 had higher serum and SF myostatin concentrations compared with those with KL grade 2. Serum and SF myostatin concentrations were significantly correlated with KL grading. Conclusion Serum and SF myostatin concentrations were correlated with the presence and severity of knee OA.

Background The aim of the study was to introduce a new percutaneous technique for the treatment of traumatic pubic symphysis diastasis using a TightRope and external fixator. A comparison between this technique and percutaneous fixation using a cannulated screw was performed. Methods From January 2009 to December 2013, 26 patients with type II traumatic pubic symphysis diastasis were treated at two level 1 regional trauma centers. Among them, 10 patients were treated with a percutaneous TightRope and external fixator and 16 patients were treated with percutaneous cannulated screw fixation. Functional outcomes were evaluated using the Majeed scoring system. Patient satisfaction was evaluated using the modified visual analog scale. Radiological results were assessed based on the width of pubic symphysis preoperatively, immediately postoperatively, and at the final follow-up. Postoperative complications were also recorded. Results There were no significant differences between the groups in Majeed scores and patient satisfaction (p > 0.05). There were no significant differences in the width of pubic symphysis preoperatively, immediately postoperatively, and at the final follow-up (p > 0.05). No significant differences were found regarding infection, fixation failure, or the need for revision surgery (p > 0.05). Conclusions The new percutaneous technique using a TightRope and external fixator is a successful alternative for the treatment of type II traumatic pubic symphysis diastasis, which results in similar outcomes comparing to percutaneous cannulated screw fixation.

The roles of different immune cell populations and cytokines in bone metabolism have been extensively investigated. However, the influence of whole immune organ removal on osteopathology remains unknown. In the current study, we investigated the effects of splenectomy on bone metabolism and microarchitecture in rats with or without concurrent ovariectomy. Ovariectomized (OVX) rats were used as osteoporosis model. Sixty 12-week-old female rats were randomized into 4 groups (n = 15): sham, splenectomized (SP), ovariectomized, as well as ovariectomized and splenectomized (OVX + SP). Bone microarchitecture was assessed by micro CT analysis at 4 week and 12 week post-operation, respectively. Bone pathology and metabolism were evaluated via immunohistochemical staining. The serum levels of alkaline phosphatase (ALP), tumor necrosis factor-alpha (TNF-α), tartrate-resistant acid phosphatase 5b (Tracp5b), and C-terminal telopeptide (CTx) were analyzed at 4 and 12 weeks post-operation. Removal of the spleen led to alterations in the homeostasis of bone metabolism and increased bone formation in rats. In this study, our findings indicate that the spleen is involved in skeletal metabolism.

Background The purpose of this study was to measure the tibiofemoral kinematics of anterior cruciate ligament (ACL) deficiency in a Chinese population and compare the kinematics with published data about a Caucasian population. Methods Unilateral knees of 18 Chinese ACL-deficient (ACL-D) subjects were studied while subjects ascended stairs. Kinematic alteration was compared between ACL-D knees and contralateral ACL-intact (ACL-I) knees. The kinematic alteration of ACL deficiency was also compared between the Chinese population and published data about a Caucasian population. Results A statistical difference was found in the three-dimensional rotations between ACL-D and ACL-I knees. In the sagittal plane, ACL-I knees had a larger flexion angle than ACL-D knees during 40 to 50 % of the activity during stair ascent (P