How to Apply Intraoperative Ultrasound when Spinal Trauma Surgery Is Performed in the Lateral Decubitus Position?

OBJECTIVE: At present, intraoperative ultrasound was widely used in spinal surgery. But there have been no reports on the use of intraoperative ultrasound in lateral decubitus position spinal surgery. The authors' research objective was to describe the applications of intraoperative ultrasound in spinal trauma surgery when performed in the lateral decubitus position. METHODS: Six patients with polytrauma who underwent surgery for spinal trauma between June 2020 and March 2022 and could not be operated on using a posterior approach in the prone position. All six patients underwent surgery in the lateral decubitus position. During surgery, a capsular bag had been designed and surgical field can be filled with normal saline for acoustic coupling, and then ultrasound was used to observe and guide decompression, and assess injuries of the neural elements such as the spinal cord. The data of preoperative and postoperative (12 months) American Spinal Injury Association impairment scale (AIS), follow-up time, operation time, blood loss, ultrasound signal change of spinal cord, ultrasound guide decompression, internal fixation (12 months), and fracture healing(12 months) were collected. RESULTS: The study included four males and two females whose ages ranged from 19 to 56 years old (41.5 ± 13.06 years old). Follow-up times ranged from 12 to 20 months (14.33 ± 2.75 months). The operation times ranged from 195 to 248 mins (222.16 ± 16.86 mins). The estimated volume of blood loss ranged from 280 to 450 mL (383.33 ± 55.58 mL). The six cases' AIS (preoperative vs. postoperative) were A versus A, C versus D, A versus B, B versus B, B versus C, and B versus C. Intraoperative ultrasound was performed successfully in all patients using our designed method. Intraoperative ultrasound observation revealed varying degrees of changes in spinal cord echo in all patients. Intraoperative ultrasound provided excellent assistance in spinal cord decompression during surgery. The surgery was completed successfully with no surgery-related complications till the last follow-up. At the time of last follow-up (median time of 12 months) satisfactory fracture reduction and good internal fixation was confirmed on postoperative computed tomography scans and radiographs. CONCLUSIONS: The authors represented the technology of intraoperative ultrasound in spinal trauma surgery when performed in the lateral decubitus position. This technology solves how to apply intraoperative ultrasound in lateral decubitus position.

Safety and Efficacy of Cortical Bone Trajectory Screw Fixation Combined with Facet Fusion for the Treatment of Lumbar Degenerative Disease.

OBJECTIVE: The mainstream lumbar fusion surgeries have various shortcomings, such as complex operation, much invasion, and loss of lumbar function. How to minimize the surgical injury and to achieve better therapeutic effects has become the goal pursued by spine surgeons. This study introduces a cortical bone trajectory (CBT) screw fixation combined with facet fusion (FF), evaluates its safety and efficacy, and explores its advantages, in order to provide a reference for treatment of patients with single-level lumbar stenosis or grade I degenerative spondylolisthesis. METHODS: We retrospectively analyzed the clinical, radiological, and operative data of 167 patients with single-level lumbar stenosis or grade I degenerative spondylolisthesis who underwent FF or transforaminal lumbar interbody fusion (TLIF) from January 2013 to September 2019 in the spine surgery department of the Second Hospital of Shandong University. Patients were divided into four groups according to surgical method: group CBT-FF, CBT screw combined with FF; group PS-FF, pedicle screw (PS) combined with FF; group CBT-TLIF, CBT screw combined with TLIF; and group PS-TLIF, PS combined with TLIF. The operation time, estimated intraoperative blood loss, complications after surgery, visual analog scale (VAS), and Oswestry disability index (ODI) of the four groups were compared. The fusion was evaluated by anteroposterior and lateral X-ray, CT scan, and three-dimensional reconstruction. RESULTS: Twelve months after surgery, the fusion rate of four groups had no significantly statistical differences (p = 0.914). VAS and ODI scores were lower after surgery than before. Low back pain VAS scores 1 week after surgery in group CBT-FF and group CBT-TLIF were significantly lower than those in group PS-FF and group PS-TLIF (pCF/PF = 0.001, pCF/PT = 0.000, pPF/CT = 0.049, pCT/PT = 0.000). Low back pain VAS score 3 months after surgery was significantly lower in group CBT-FF than group PS-FF and group PS-TLIF (pCF/PF = 0.045, pCF/PT = 0.008). ODI score 1 week after surgery was significantly lower in group CBT-FF than group PS-FF, group CBT-TLIF, and group PS-TLIF (pCF/PF = 0.000, pCF/CT = 0.005, pCF/PT = 0.000, pCT/PT = 0.015). ODI score 3 months after surgery was significantly lower in group CBT-FF than group PS-FF, group CBT-TLIF, and group PS-TLIF (pCF/PF = 0.001, pCF/CT = 0.002, pCF/PT = 0.000). Incidence of complications did not significantly differ among the groups. CONCLUSION: CBT screw fixation combined with FF is a safe and efficacious procedure for patients with single-level lumbar stenosis or grade I degenerative spondylolisthesis. This minimally invasive approach of lumbar fusion can be simply and easily performed. Patients who undergo CBT screw fixation combined with FF recovered faster than TLIF.

Immune-based prognostic biomarkers associated with metastasis of osteosarcoma.

This study aimed to identify immune-based prognostic biomarkers associated with metastasis of osteosarcoma. Based on the GEO and TCGA databases, 437 differentially expressed genes were screened between primary and metastatic osteosarcoma. Weighted gene co-expression network analysis (WGCNA) revealed 496 genes in turquoise module which had the highest correlation with osteosarcoma metastasis. Within these two group genes, 122 common genes involved in osteosarcoma metastasis were identified. These genes were enriched in chemokine activity, chemokine receptor binding, TNF signaling pathway, etc. Survival analysis revealed 8 prognostic genes (ANK3, EGR1, FBP1, FOS, KIFC3, MAOB, ISLR and MFAP4) from the 122 genes. RT-qPCR showed that all of these eight genes were differentially expressed between 143B and MNNG/HOS Cl cells. Various infiltrating immune cells showed significant differences between primary and metastatic osteosarcoma. Expression of all the 8 prognostic genes was correlated with infiltration abundance of multiple immune cells, such as follicular helper T cells, activated dendritic cells. In addition, 10 microRNAs and 7 transcription factors that targeted these prognostic genes were predicted. In conclusion, 8 immune-based prognostic genes associated with osteosarcoma metastasis were identified.

Diagnostic value of curved planar reformation of MRI for lumbosacral nerve roots in the localization of nerve roots for adult lumbar degenerative scoliosis.

PURPOSE: To compare the diagnostic value of curved planar reformation of MRI (MRI-CPR) and 2D MRI in determining the responsible nerve in patients with adult lumbar degenerative scoliosis (ALDS). METHOD: A total of 45 patients diagnosed with ALDS were included in the study. All patients underwent MRI-CPR and 2D MRI and subsequently received surgery. These two diagnostic methods were compared with the results of surgical exploration to assess nerve root compression. RESULTS: The sensitivity and accuracy of MRI-CPR are higher than 2D MRI (93.8% vs 80.0%; 92.8% vs 77.7%, respectively). And the specificity of MRI-CPR is higher than 2D MRI (87.5% vs 68.8%). Besides, the PPV and NPV of MRI-CPR are higher than 2D MRI (96.8% vs 91.2%; 7.8.% vs 45.8%). The area (AUC) under the receiver operating characteristic curve (ROC) for MRI-CPR and 2D MRI was 0.74 and 0.91, respectively. The judgement was made by two independent radiologists, while the consistency tests for 2D MRI and MRI-CPR with Kappa values were 90.6% and 82.2%, respectively. CONCLUSIONS: The clinical diagnostic value of MRI-CPR was better than 2D MRI in the determination of the responsible nerve root. Moreover, MRI-CPR sequence images can clearly show the route of lumbosacral nerve roots and their relationship with adjacent tissues. Therefore, MRI-CPR can be an important complement to conventional 2D MRI in the diagnosis of responsible nerve roots in patients with ALDS.

The influence of carotid atherosclerosis on surgical outcomes of patients with cervical spondylotic myelopathy: A retrospective study.

ABSTRACT: The appearance of atherosclerosis in the carotid artery may be suggest the possibility of atherosclerosis in the spinal cord artery, which can cause spinal cord ischemia and further lead to neural element damage.According to the inclusion and exclude standard, there are 137 patients with cervical spondylotic myelopathy (CSM) incorporating retrospective analysis. These patients were consecutively admitted into The Second Hospital- Cheeloo College of Medicine-Shandong University from January 2016 to December 2018 and have accepted surgical treatment. All patients were examined by color Doppler ultrasound to detect carotid atherosclerosis before surgery. All patients were divided into 2 groups according to the presence or absence of carotid atherosclerosis: carotid atherosclerosis group (n = 88) and noncarotid atherosclerosis group (n = 49). All patients were followed up for at least 12 months after surgery. Demographic and surgery-related data were collected and analyzed to identify potential factors that affect the surgical outcomes in CSM.The average age of carotid atherosclerosis group (51 males and 37 females), and noncarotid atherosclerosis group (24 males and 25 females) were 62.02 ±â€Š10.34 years (range, 38-85 years) and 49.61 ±â€Š10.28 years (range, 26-67 years), respectively.In carotid atherosclerosis group: pre and postoperative modify Japanese Orthopedic Association Scores (mJOA score) were 11.58 ±â€Š1.82 and 14.36 ±â€Š1.64; the recovery rate of mJOA score was 45.57% ±â€Š13.28%. In noncarotid atherosclerosis group: pre and postoperative mJOA score were 12.00 ±â€Š2.11 and 15.04 ±â€Š1.70; the recovery rate of mJOA score was 53.90% ±â€Š13.22%. Univariate logistic regression analysis demonstrated that gender (P = .004), age ≥65 years (P = .001), duration of symptoms ≥12 months (P = .040), smoking history (P < .001), preoperative mJOA score ≤11 (P = .007) and carotid atherosclerosis (P = .004) were related to poor surgical outcomes. Multivariate logistic regression analysis showed significant correlations between poor surgical outcomes and age ≥65 years (P = .047), smoking history (P = .010), preoperative mJOA score ≤11 (P = .008) or carotid atherosclerosis (P = .047).Carotid atherosclerosis may be a risk factor for poor surgical outcomes in CSM.

Neuropeptide Y upregulates Runx2 and osterix and enhances osteogenesis in mouse MC3T3­E1 cells via an autocrine mechanism.

The neuropeptide Y (NPY) system is considered one of the primary neural signaling pathways. NPY, produced by osteoblasts and other peripheral tissues, is known to inhibit biological functions of osteoblasts. However, until recently, little was known of the autocrine mechanism by which NPY is regulated. To investigate this mechanism, overexpression plasmids and small interfering RNA (siRNA) targeting NPY were transfected into the MC3T3­E1 cell line to observe its effects on osteogenesis. NPY overexpression was found to markedly enhance the osteogenic ability of MC3T3­E1 cells by an autocrine mechanism, coincident with the upregulation of osterix and runt­related transcription factor 2 (Runx2). Furthermore, NPY increased the activities of alkaline phosphatase (ALP) and osteocalcin (OCN) by upregulating their osteoblastic expression in vitro (as well as that of osterix and Runx2). Following transfection with NPY­siRNA, the osteoblastic ability of MC3T3­E1 cells was markedly decreased, and NPY deficiency inhibited the protein expression of osterix, Runx2, OCN and ALP in primary osteoblasts. Collectively, these results indicated that NPY played an important role in osteoblast differentiation by regulating the osterix and Runx2 pathways.

MicroRNA-618 Directly Targets Metadherin mRNA To Suppress The Malignant Phenotype Of Osteosarcoma Cells By Reducing PTEN-AKT Pathway Output.

PURPOSE: Dysregulation of microRNA-618 (miR-618) has been observed in multiple types of human cancer. However, whether miR-618 is implicated in osteosarcoma (OS) initiation and progression is still unclear. Hence, we measured the expression of miR-618 in OS tissues and cell lines. In addition, the roles of miR-618 and the mechanisms underlying its activities in OS cells were examined. METHODS: The expression status of miR-618 in OS was analyzed by reverse-transcription quantitative PCR. The regulatory roles of miR-618 overexpression in OS were explored by the Cell Counting Kit-8 assay, flow-cytometric analysis, Transwell cell migration and invasion assays, and a tumor xenograft experiment. RESULTS: The results revealed that the expression of miR-618 was notably lower in OS tissues and cell lines, and that the low miR-618 expression significantly correlated with the clinical stage and distant metastasis among patients with OS. Exogenous miR-618 expression significantly suppressed OS cell proliferation, migration, and invasion and induced apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation indicated that metadherin (MTDH) is a direct target gene of miR-618 in OS cells. A knockdown of MTDH mimicked the tumor-suppressive effects of miR-618 upregulation on OS cells. Notably, resumption of MTDH expression attenuated the miR-618-mediated reduction in OS cell growth and metastasis in vitro. In addition, miR-618 overexpression reduced the PTEN-AKT pathway output in OS cells both in vitro and in vivo through downregulation of MTDH. CONCLUSION: To the best of our knowledge, this is the first study to show that miR-618 exerts crucial tumor-suppressive actions in OS pathogenesis by directly targeting MTDH mRNA and reducing PTEN-AKT pathway output. These results will help to elucidate the functions of miR-618 in OS and suggest that this miRNA may be investigated as a therapeutic target in this disease.

G-CSF Inhibits Growths of Osteoblasts and Osteocytes by Upregulating Nitric Oxide Production in Neutrophils.

OBJECTIVE: Granulocyte colony-stimulating factor (G-CSF) is the critical regulator of the proliferation, differentiation, and survival of granulocytes. Recently, it has been shown that G-CSF can adversely affect bone health in both animal models and patients. Here, the authors aimed to investigate whether G-CSF could inhibit the growth of osteoblasts and osteocytes by regulating nitric oxide. METHODS: The C57BL/6 mice were divided into the control group, G-CSF treatment group and recovery group (G-CSF+L-NAME). The morphology of femurs was assessed by histology and immunohistochemistry. The expression of apoptosis-related molecules in femurs was detected by immunohistochemistry and quantitative RT-PCR, respectively. To examine if neutrophil-secreted factors can induce apoptosis in osteoblasts, Gr1-positive (Gr1+) neutrophils from the bone marrow of wild-type mice were sorted and co-cultured with MC3T3 pre-osteoblasts for 2 days. RESULTS: The number of osteoblasts and newly embedding osteocytes significantly decreased and markers related to osteoblasts and osteocytes were downregulated in the G-CSF treatment compared to the control group. Moreover, G-CSF treatment did not change proliferation markers but induced apoptosis in osteoblast-lineage cells. The combined treatment of mice with G-CSF and a nitric oxide inhibitor partially restored the number of osteoblasts and osteocyte parameters. CONCLUSIONS: The G-CSF can inhibit osteoblasts and osteocytes by upregulating nitric oxide.

Long non-coding RNA highly up-regulated in liver cancer protects tumor necrosis factor-alpha-induced inflammatory injury by down-regulation of microRNA-101 in ATDC5 cells.

BACKGROUND: Osteoarthritis (OA) is a familiar joint degenerative disease. Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis of OA. Nevertheless, the regulatory impacts of lncRNA highly up-regulated in liver cancer (lncRNA-HULC) on OA remain dimness. The study tried to probe the protective effect of HULC on ATDC5 cells against tumor necrosis factor-alpha (TNF-α)-induced inflammatory injury. METHODS: Relative expression levels of pro-inflammatory cytokines (IL-6, IL-8 and MCP-1) and HULC in OA cartilage tissues and normal cartilage tissues were determined by RT-qPCR. TNF-α induced inflammatory injury model in ATDC5 cells was constructed, and the biological functions of HULC overexpression or suppression in TNF-α-injured ATDC5 cells were assessed. The relevancy between miR-101 and HULC was investigated by utilizing bioinformatics prediction, luciferase reporter assay, RNA pull-down and immunoprecipitation. MiR-101 mimic and inhibitor were transfected into ATDC5 cells, and its regulatory effect on TNF-α-injured ATDC5 cells was examined. Further, NF-κB and MAPK signaling pathways were finally detected by western blot. RESULTS: Enhancement of IL-6, IL-8 and MCP-1 were observated in OA cartilage tissues, but repression of HULC was discovered in OA cartilage tissues. HULC expression was decreased by TNF-α treatment, and overexpressed HULC significantly relieved TNF-α-induced ATDC5 cells injury. Additionally, miR-101 was mutual repressed with HULC, and overexpressed miR-101 reversed the protective effect of HULC in TNF-α-injured ATDC5 cells. Besides, HULC blocked NF-κB and MAPK pathways via repression of miR-101. CONCLUSIONS: The discoveries testified that HULC protected ATDC5 cells against TNF-α-induced inflammatory injury by repression of miR-101.

Blocking of checkpoint receptor PD-L1 aggravates osteoarthritis in macrophage-dependent manner in the mice model.

As a chronic degenerative joint disease, osteoarthritis is among the most common diseases all over the world. In osteoarthritis, inflammation plays an important role in the generation of joint symptoms and the development of disease. When the programmed cell death-1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint is blocked, the antitumor immunity will be enhanced. We aim to illustrate the function of PD-L1 in osteoarthritis. Osteoarthritis in mice was induced by the injection of collagenase or anterior cruciate ligament transection (ACLT). Anti-PD-L1 was employed to block the signal of PD-L1. Knee joints histological sections were stained by Safranin-O. The level of cytokine was checked by enzyme-linked immunosorbent assay (ELISA) and mRNA level was shown by quantitative reverse transcriptase polymerase chain reaction. The blockade of PD-L1 signal up-regulated inflammatory response and promoted the development of osteoarthritis in mice. The inflammatory cytokine interleukin-6 and tumor necrosis factor-α expression were promoted by PD-L1 blocking in macrophages. Osteoarthritis was aggravated when the expression of inflammatory cytokine is elevated in macrophages. Our results indicated that the blockade of PD-L1 signal in macrophages elevates the expression of inflammatory cytokine and promotes the development of osteoarthritis in mice, which could be utilized as a potential diagnostic and therapeutic target for osteoarthritis patients.

FLVCR1 promotes the proliferation and tumorigenicity of synovial sarcoma through inhibiting apoptosis and autophagy.

Feline leukemia virus subgroup C receptor 1 (FLVCR1) has been reported to have a crucial role in variety of biological processes, including cell proliferation, cell death, apoptosis, oxidative stress response, cellular differentiation and metabolism. However, little is known about its role in synovial sarcoma (SS). In the current study, FLVCR1 expression was analyzed in two SS cell lines (SW982 and HS-SY-II), and in eight SS tissues and paired adjacent non-tumor tissues using reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry. Lentivirus-mediated short hairpin RNAs were used to knock down FLVCR1 expression in SW982 and HS-SY-II cells. The effects of FLVCR1 knockdown on the cell proliferation, clonogenicity, cell cycle and apoptosis in SS cells were evaluated by MTT, colony formation assay, flow cytometry analysis, western blotting and in vivo tumorigenesis in nude mice. In the current study, gene expression of FLVCR1 was upregulated in SS cell lines (SW982 and HS-SY-II) and SS tissues from patients. The protein levels of FLVCR1 in SS tissues were also significantly higher than in adjacent non-tumor tissues. Furthermore, suppressing the expression of FLVCR1 in SS cells using short hairpin RNA effectively attenuated cell proliferation, colony formation and impaired the cell cycle, and also significantly induced apoptosis and autophagy. In accordance with this, an in vivo tumorigenicity assay in mice demonstrated that suppression of FLVCR1 expression inhibited the growth of SS tumors implanted subcutaneously. Collectively, these results demonstrated that FLVCR1 may act as an oncoprotein, and have key roles in promoting proliferation and tumorigenicity of SS, and this may shed new light on finding novel therapeutic strategies against SS.

miRNA-20a upregulates TAK1 and increases proliferation in osteosarcoma cells.

AIM: The aim of this study is to explore the function of miR-20a in osteosarcoma. MATERIALS & METHODS: miR-20a expression was measured by real-time PCR. miR-20a mimics, inhibitor and scramble siRNA were transfected into osteosarcoma cells to observe effects on colony formation and tumor growth. Moreover, relationships of miR-20a with TAK1 were investigated by western blot and luciferase activity. RESULTS: We found that miR-20a was downregulated in osteosarcoma, and overexpression of miR-20a reduced colony formation and tumor growth. Furthermore, the data revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. Overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs. CONCLUSION: Our data identify the role of miR-20a in osteosarcoma growth, indicating its potential application in chemotherapy.

Bindarit Attenuates Pain and Cancer-Related Inflammation by Influencing Myeloid Cells in a Model of Bone Cancer.

C-C motif chemokine ligand 2 (CCL2) is a small cytokine that functions in inflammation and cancer development. Bindarit, a CCL2 inhibitor, is a small anti-inflammatory molecule proven safe by phase II trials in type 2 diabetic nephropathy patients. As cancer-related inflammation is a cause of pain, we investigated whether Bindarit suppresses cancer-related inflammation and pain. We established a bone-cancer mouse model by inoculating cancer cells. After applying Bindarit, we preformed pain sensitivity tests and checked cancer development by X-ray. Using flow cytometry and qRT-PCR assays, we assessed the effect of Bindarit on peripheral blood monocyte mobilization and M2 macrophage polarization. We also investigated the targets of Bindarit using western blotting and luciferase assay. Bindarit-treated mice performed better in pain sensitivity tests compare to control mice. X-ray imaging showed that Bindarit-treated mice had fewer cancer cell colonies and smaller overall tumor burden. Bindarit reduced the number of monocytes in peripheral blood and down-regulated the expression of M2 macrophage polarization makers. Bindarit also inhibited IKKß phosphorylation. Bindarit efficiently relieves cancer-related pain and suppresses cancer development. Bindarit inhibits monocyte mobilization in peripheral blood as well as M2 macrophage polarization. IKKß is identified as a target of Bindarit.

SHCBP1 promotes synovial sarcoma cell metastasis via targeting TGF-ß1/Smad signaling pathway and is associated with poor prognosis.

BACKGROUND: Our previous studies reported that SHC SH2-domain binding protein 1 (SHCBP1) functions as an oncogene via promoting cell proliferations in synovial sarcoma (SS) cells. However, whether SHCBP1 has any effect on tumor metastasis remains unexplored. METHODS: The expression of SHCBP1 was analyzed in 76 SS tissues and two SS cell lines by immunohistochemistry and real-time RT-PCR. The relationship between SHCBP1 expression and the clinicopathological features of SS was investigated. The role of SHCBP1 in SS cell adhesion, migration, invasion and angiogenesis was explored by adhesion, Wound healing, Transwell, and Matrigel tube formation assays. Western blotting was conducted to detect the protein expressions of TGF-ß1/Smad signaling pathway and EMT-related markers. The key molecules associated with migration, invasion and EMT were evaluated by immunohistochemistry in tumor specimens. RESULTS: In current study, we demonstrated that SHCBP1 overexpression significantly enhanced adhesion, migration, invasion and angiogenesis of SS cells. In contrast, SHCBP1 knockdown elicited the opposite effects on these phenotypes in vitro. SHCBP1 promoted tumor metastasis through inducing epithelial-mesenchymal transition (EMT) in SS cells. SHCBP1 knockdown could block the incidence of metastasis and EMT in SS cells. Furthermore, transforming growth factor-ß1 (TGF-ß1) induced SHCBP1 expression in a time-dependent pattern and SHCBP1 knockdown inhibited TGF-ß1-induced EMT. The activation of the TGF-ß1/Smad signaling pathway was involved in the oncogenic functions of SHCBP1 in SS. In addition, high expression of SHCBP1 in SS patients was associated with tumor progression and decreased survival as well as poor prognosis. CONCLUSIONS: Taken together, our results indicate that SHCBP1 may promote the metastasis of SS by inducing EMT through targeting TGF-ß1/Smad signaling pathway and can be a potential molecular target for SS therapy.

Neoadjuvant chemotherapy combined with limb salvage surgery in patients with limb osteosarcoma of Enneking stage II: a retrospective study.

OBJECTIVE: To explore the effect of neoadjuvant chemotherapy combined with limb salvage surgery in patients with limb osteosarcoma of Enneking stage II. PATIENTS AND METHODS: Medical records of 98 patients who met the inclusion criteria were retrospectively analyzed. Of these patients, 56 cases who received neoadjuvant chemotherapy combined with limb salvage surgery were listed as group A, while another 42 patients who received limb salvage surgery combined with adjuvant chemotherapy were listed as group B. The recurrence and metastasis rate, survival rate, limb function and incidence of adverse reactions were compared between the two groups. RESULTS: All 98 patients completed the treatment in this study. Baseline characteristics showed no significant differences between group A and group B, including age, gender, tumor location, maximum tumor diameter and Enneking stage (all P>0.05). The total metastasis and recurrence rate of group A was significantly lower than that of group B (25.0% vs 47.6%, χ2=5.419, P=0.020). The Kaplan-Meier method showed that progression-free survival (PFS) (log-rank χ2=4.014, P=0.045) and overall survival (OS) (log-rank χ2=3.859, P=0.049) of group A were both significantly higher than those of group B. There was no significant difference in the incidence of grades III-IV adverse reactions between the two groups (all P>0.05). The excellent and good rate of limb function in group A was significantly higher than that in group B (83.9% vs 66.7%, χ2=3.982, P=0.046). CONCLUSION: Neoadjuvant chemotherapy combined with limb salvage surgery for patients with Enneking stage IIA or IIB limb osteosarcoma patients has better efficacy and can significantly improve limb function of patients.

Mir-150 Up-Regulates Glut1 and Increases Glycolysis in Osteosarcoma Cells

Objective: Osteosarcoma (OS) is the most common malignant bone tumor in children and young adults. Many studies have shown that microRNAs play a critical role in proliferation and metastasis with this tumour type. However, whether aberrant expression might contribute to a metabolism switch in osteosarcoma cases is not clearly understood. In this study, we explored expression and function of miR-150 in osteosarcoma cells. Materials and methods: Expression of miR-150 was assessed by real-time PCR in cell lines and human patient tissues. Scramble siRNA, miR-150 inhibitor, and miR-150 mimics were transfected into osteosarcoma cells to determine their effects on proliferation rate, glucose uptake and lactate secretion. Finally, the relationship between Glut1 and the miR-150 level was explored by luciferase reporter assay and western blotting. Result: miR-150 was consistently decreased in cell lines and osteosarcoma tissues as compared to osteoblast cells and normal bone. Ectopic overexpression of miR-150 inhibited osteosarcoma cell proliferation and suppressed glucose uptake and lactate secretion. Loss of function of miR-150, on the other hand, enhanced osteosarcoma cell proliferation and increased glucose uptake and lactate secretion. Western blot and luciferase reporter assays showed that miR-150 may function by regulating Glut1 expression. Conclusion: These data suggest that miR-150 is involved in regulation of glycolysis in osteosarcoma cells by influencing Glut1 expression.

Anatomical study of the coracoid process in Mongolian male cadavers using the Latarjet procedure.

BACKGROUND: The Latarjet procedure addresses recurrent anterior shoulder instability in the context of a significant bony defect. However, the bony and soft tissue anatomy of the coracoid in coracoid transfer procedures has not yet been defined in Mongolian men. The aims of this study were to describe the soft tissue attachments of the coracoid regarding the bony anatomy, define the average amount of bone available for coracoid transfer, analyze the characteristics of the pectoralis minor and coracoid, and study the relationship between the bony dimensions of the coracoid and body length in Mongolian men. METHODS: We dissected 30 shoulders from 15 male Mongolian cadavers, exposing the coracoid process and attached anatomical structures including the lateral clavicle and acromion, then measured the bony dimensions of the coracoid and the locations and sizes of the coracoid soft tissue footprints. RESULTS: The mean length of the coracoid available for transfer was 23.93 ± 2.32 mm. The mean length of the coracoid was 42.10 ± 2.3 mm, and the mean width and height of the coracoid midpoint were 15.29 ± 1.70 mm and 11.61 ± 1.98 mm, respectively. The pectoralis minor was part of the joint capsule and passed over the coracoid in some samples. The mutation rate of the pectoralis minor footprint, which was asymmetrical and irregular, was 23.33 %. Statistical analysis involved a multiple linear regression equation. CONCLUSIONS: The average amount of bone available for use in coracoid transfer in Mongolian men was less than that of other populations. Mutation of the pectoralis minor may induce intraoperative capsule injury because this muscle passes over the coracoid deep to the joint capsule of the glenohumeral joint and constitutes part of the shoulder joint, strengthening the joint. Statistically, higher coracoids appeared in shorter patients and longer coracoids appeared in taller patients. Surgically, great care should be taken to consider a patient's height to precisely implement the congruent-arc Latarjet technique.

Identification of SHCBP1 as a novel downstream target gene of SS18-SSX1 and its functional analysis in progression of synovial sarcoma.

The SS18-SSX1 fusion gene has been shown to play important roles in the development of synovial sarcoma (SS), but the underlying molecular mechanisms and its downstream target genes are still not clear. Here SHC SH2-domain binding protein 1 (SHCBP1) was identified and validated to be a novel downstream target gene of SS18-SSX1 by using microarray assay, quantitative real-time (qPCR) and western blot. Expression of SHCBP1 was firstly confirmed in SS cell line and SS tissues. The effects of SHCBP1 overexpression or knockdown on SS cell proliferation and tumorigenicity were then studied by cell proliferation, DNA replication, colony formation, flow cytometric assays, and its in vivo tumorigenesis was determined in the nude mice. Meanwhile, the related signaling pathways of SHCBP1 were also examined in SS cells. The results indicated that SHCBP1 was significantly increased in SS cells and SS tissues compared with adjacent noncancerous tissues. The expression of SHCBP1 was demonstrated to be positively correlated with the SS18-SSX1 level. Overexpression and ablation of SHCBP1 promoted and inhibited, respectively, the proliferation and tumorigenicity of SS cells in vitro. SHCBP1 knockdown also significantly inhibited SS cell growth in nude mice, and lowered the MAPK/ERK and PI3K/AKT/mTOR signaling pathways and cyclin D1 expression. Our findings disclose that SHCBP1 is a novel downstream target gene of SS18-SSX1, and demonstrate that the oncogene SS18-SSX1 promotes tumorigenesis by increasing the expression of SHCBP1, which normally acts as a tumor promoting factor.

Defective Function of CD24(+)CD38(+) Regulatory B Cells in Ankylosing Spondylitis.

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease strongly associated with HLA-B*27, an major histocompatibility complex (MHC) molecule that presents peptide antigen to T cells. Previously, regulatory B cells were found to suppress T cell-mediated autoimmunity induction and chronic inflammation, partially through interleukin (IL)-10 production. Here, we examined the role of regulatory B cells in AS pathogenesis. Apheresis samples from HLA-B*27-positive AS patients and non-AS healthy controls were collected. We found that although AS patients and non-AS controls presented similar frequencies of CD24(+)CD38(+) B cells, compared to non-AS controls, those from AS patients produced less IL-10 under ex vivo condition and after CD40 and B-cell receptor (BCR) stimulation. Purified T cell-B cell cocultures showed that compared to non-AS controls, CD24(+)CD38(+) B cells from AS patients were defective at suppressing naive and memory CD8(+) T cell activation. The suppression of memory CD8(+) T cells in non-AS controls appeared to be mediated by IL-10, since the addition of IL-10 mAb suppressed CD24(+)CD38(+) B cell-mediated downregulation of proinflammatory cytokine production and proliferation. To rescue the defect in AS patients, CD24(+)CD38(+) B cells were pretreated by CD40 and BCR stimulation, which enhanced CD24(+)CD38(+) B cell-mediated memory CD8(+) T cell suppression. Together, our data discovered a regulatory B cell defect in AS patients.