Incidence and risk factors of proximal junctional kyphosis in adolescent idiopathic scoliosis after correction surgery: a meta-analysis and systematic review.

AIM: To analyze the risk factors of proximal junctional kyphosis (PJK) after correction surgery in patients with adolescent idiopathic scoliosis (AIS). METHODS: PubMed, Medline, Embase, Cochrane Library, Web of Science, CNKI, and EMCC databases were searched for retrospective studies utilizing all AIS patients with PJK after corrective surgery to collect preoperative, postoperative, and follow-up imaging parameters, including thoracic kyphosis (TK), lumbar lordosis (LL), proximal junctional angle (PJA), the sagittal vertical axis (SVA), pelvic incidence (PI), pelvic tilt (PT), pelvic incidence-lumbar lordosis (PI-LL), sacral slope (SS), rod contour angle (RCA) and upper instrumented vertebra (UIV). RESULTS: Nineteen retrospective studies were included in this meta-analysis, including 550 patients in the intervention group and 3456 patients in the control group. Overall, sex (OR 1.40, 95% CI (1.08, 1.83), P = 0.01), larger preoperative TK (WMD 6.82, 95% CI (5.48, 8.16), P < 0.00001), larger follow-up TK (WMD 8.96, 95% CI (5.62, 12.30), P < 0.00001), larger postoperative LL (WMD 2.31, 95% CI (0.91, 3.71), P = 0.001), larger follow-up LL (WMD 2.51, 95% CI (1.19, 3.84), P = 0.0002), great change in LL (WMD - 2.72, 95% CI (- 4.69, - 0.76), P = 0.006), larger postoperative PJA (WMD 4.94, 95% CI (3.62, 6.26), P < 0.00001), larger follow-up PJA (WMD 13.39, 95% CI (11.09, 15.69), P < 0.00001), larger postoperative PI-LL (WMD - 9.57, 95% CI (- 17.42, - 1.71), P = 0.02), larger follow-up PI-LL (WMD - 12.62, 95% CI (- 17.62, - 7.62), P < 0.00001), larger preoperative SVA (WMD 0.73, 95% CI (0.26, 1.19), P = 0.002), larger preoperative SS (WMD - 3.43, 95% CI (- 4.71, - 2.14), P < 0.00001), RCA (WMD 1.66, 95% CI (0.48, 2.84), P = 0.006) were identified as risk factors for PJK in patients with AIS. For patients with Lenke 5 AIS, larger preoperative TK (WMD 7.85, 95% CI (5.69, 10.00), P < 0.00001), larger postoperative TK (WMD 9.66, 95% CI (1.06, 18.26), P = 0.03, larger follow-up TK (WMD 11.92, 95% CI (6.99, 16.86), P < 0.00001, larger preoperative PJA (WMD 0.72, 95% CI (0.03, 1.41), P = 0.04, larger postoperative PJA (WMD 5.54, 95% CI (3.57, 7.52), P < 0.00001), larger follow-up PJA (WMD 12.42, 95% CI 9.24, 15.60), P < 0.00001, larger follow-up SVA (WMD 0.07, 95% CI (- 0.46, 0.60), P = 0.04), larger preoperative PT (WMD - 3.04, 95% CI (- 5.27, - 0.81), P = 0.008, larger follow-up PT (WMD - 3.69, 95% CI (- 6.66, - 0.72), P = 0.02) were identified as risk factors for PJK. CONCLUSION: Following corrective surgery, 19% of AIS patients experienced PJK, with Lenke 5 contributing to 25%. Prior and post-op measurements play significant roles in predicting PJK occurrence; thus, meticulous, personalized preoperative planning is crucial. This includes considering individualized treatments based on the Lenke classification as our future evaluation standard.

Process Optimization of SiC-Reinforced Aluminum Matrix Composites Prepared Using Laser Powder Bed Fusion and the Effect of Particle Morphology on Performance.

Process parameters and powder spreading quality are important factors for aluminum matrix composites (AMCs) prepared using laser powder bed fusion (LPBF). In this study, a Box-Behnken Design (BBD) was used to optimize the process parameters, and near-spherical ß-SiC was selected to improve the quality of powder spreading. The rationality of parameter optimization was verified by testing the density of samples prepared using different laser power levels. Al4C3 diffraction peaks were found in XRD patterns, which indicated that interface reactions occurred to form good interface bonding between the Al matrix and the SiC particles. The tensile strength and plasticity of LPBF α-SiC/AlSi10Mg were lower than that of LPBF AlSi10Mg, which was mainly due to the poor fluidity of the powder mixtures and powder spreading quality. For LPBF ß-SiC/AlSi10Mg, the tensile strength increased and elongation decreased slightly compared to LPBF α-SiC/AlSi10Mg. The data in this study were compared with the data in other studies. In this study, LPBF AlSi10Mg and LPBF ß-SiC/AlSi10Mg not only showed the inherent high strength of their LPBF parts, but also had relatively high plasticity. Matching between strength and plasticity was mainly dependent on the scanning strategy. Most studies use uni-directional or bi-directional scanning strategies with a certain rotation angle between layers. A chessboard scanning strategy was used in this study to form a coarse remelted connected skeleton inside the material and significantly improve plasticity. This study lays a theoretical and experimental foundation for the controllable preparation of SiC-reinforced AMCs using LPBF.

Machine learning algorithm predicts fibrosis-related blood diagnosis markers of intervertebral disc degeneration.

BACKGROUND: Intervertebral disc cell fibrosis has been established as a contributing factor to intervertebral disc degeneration (IDD). This study aimed to identify fibrosis-related diagnostic genes for patients with IDD. METHODS: RNA-sequencing data was downloaded from Gene Expression Omnibus (GEO) database. The diagnostic genes was identified using Random forest based on the differentially expressed fibrosis-related genes (DE-FIGs) between IDD and control samples. The immune infiltration states in IDD and the regulatory network as well as potential drugs targeted diagnostic genes were investigated. Quantitative Real-Time PCR was conducted for gene expression valifation. RESULTS: CEP120 and SPDL1 merged as diagnostic genes. Substantial variations were observed in the proportions of natural killer cells, neutrophils, and myeloid-derived suppressor cells between IDD and control samples. Further experiments indicated that AC144548.1 could regulate the expressions of SPDL1 and CEP120 by combininghsa-miR-5195-3p and hsa-miR-455-3p, respectively. Additionally, transcription factors FOXM1, PPARG, and ATF3 were identified as regulators of SPDL1 and CEP120 transcription. Notably, 56 drugs were predicted to target these genes. The down-regulation of SPDL1 and CEP120 was also validated. CONCLUSION: This study identified two diagnostic genes associated with fibrosis in patients with IDD. Additionally, we elucidated their potential regulatory networks and identified target drugs, which offer a theoretical basis and reference for further study into fibrosis-related genes involved in IDD.

GREM1, LRPPRC and SLC39A4 as potential biomarkers of intervertebral disc degeneration: a bioinformatics analysis based on multiple microarray and single-cell sequencing data.

BACKGROUND: Low back pain (LBP) has drawn much widespread attention and is a major global health concern. In this field, intervertebral disc degeneration (IVDD) is frequently the focus of classic studies. However, the mechanistic foundation of IVDD is unclear and has led to conflicting outcomes. METHODS: Gene expression profiles (GSE34095, GSE147383) of IVDD patients alongside control groups were analyzed to identify differentially expressed genes (DEGs) in the GEO database. GSE23130 and GSE70362 were applied to validate the yielded key genes from DEGs by means of a best subset selection regression. Four machine-learning models were established to assess their predictive ability. Single-sample gene set enrichment analysis (ssGSEA) was used to profile the correlation between overall immune infiltration levels with Thompson grades and key genes. The upstream targeting miRNAs of key genes (GSE63492) were also analyzed. A single-cell transcriptome sequencing data (GSE160756) was used to define several cell clusters of nucleus pulposus (NP), annulus fibrosus (AF), and cartilaginous endplate (CEP) of human intervertebral discs and the distribution of key genes in different cell clusters was yielded. RESULTS: By developing appropriate p-values and logFC values, a total of 6 DEGs was obtained. 3 key genes (LRPPRC, GREM1, and SLC39A4) were validated by an externally validated predictive modeling method. The ssGSEA results indicated that key genes were correlated with the infiltration abundance of multiple immune cells, such as dendritic cells and macrophages. Accordingly, these 4 key miRNAs (miR-103a-3p, miR-484, miR-665, miR-107) were identified as upstream regulators targeting key genes using the miRNet database and external GEO datasets. Finally, the spatial distribution of key genes in AF, CEP, and NP was plotted. Pseudo-time series and GSEA analysis indicated that the expression level of GREM1 and the differentiation trajectory of NP chondrocytes are generally consistent. GREM1 may mainly exacerbate the degeneration of NP cells in IVDD. CONCLUSIONS: Our study gives a novel perspective for identifying reliable and effective gene therapy targets in IVDD.

Upper trapezius muscle elasticity in cervical myofascial pain syndrome measured using real-time ultrasound shear-wave elastography.

Background: Myofascial pain syndrome (MPS) is a common cause of neck pain, which is a global public health problem. Because MPS does not present morphological changes within lesioned muscles, there are no imaging diagnostic criteria for this condition. In this study, we evaluate elasticity changes in upper trapezius muscles most frequently involved in cervical MPS using real-time ultrasound shear-wave elastography, and we examine their potential diagnostic value. Methods: We consecutively enrolled 109 right posterior neck pain patients for this prospective study. Of these, 51 were diagnosed with MPS and 58 with non-MPS in the right side of their neck. Among MPS patients, 19 fell into the 1-3 range (mild pain) for pain scores on the visual analog scale (VAS), 25 fell into the 4-6 range (moderate pain), and 7 into the 7-10 range (severe pain). MPS was diagnosed by two independent clinicians using the diagnostic criteria proposed by Simons et al. Using real-time ultrasound shear-wave elastography, we measured right trapezius mean shear-wave velocity (SWVmean). The midpoint of the line between the foramen magnum and the end of the right acromion served as measuring point. Regions of interest were scaled to span 0-8.0 m/s. Results: Trapezius SWVmean was significantly higher in MPS patients compared with non-MPS patients (P<0.001). Stratified analysis of MPS patients according to pain severity revealed similar trapezius SWVmean between mild pain and non-MPS patients (P=0.324), however SWVmean was higher in moderate and severe pain MPS patients compared with non-MPS patients (P<0.001). The area under the curve (AUC) value for upper trapezius SWVmean in MPS patients was 0.791 (95% CI: 0.703-0.863). Corresponding sensitivity and specificity values were 86.27% (95% CI: 73.7-94.3%) and 62.07% (95% CI: 48.4-74.5%). Stratified analysis of MPS patients by pain severity produced the following AUC values for trapezius SWVmean in MPS patients with mild, moderate, and severe pain: 0.578 (95% CI: 0.460-0.690), 0.899 (95% CI: 0.814-0.955), and 0.983 (95% CI: 0.914-0.999), respectively. Conclusions: Elasticity changes and increased stiffness in the trapezius occur in cervical MPS patients with moderate and severe pain. The SWVmean parameter reflecting trapezius muscle elasticity may be valuable for successful screening of cervical MPS, especially in patients with moderate and severe pain.

Extraskeletal myxoid chondrosarcoma of the buttock: a case report and literature review.

Background: Extraosseous myxoid chondrosarcoma (EMC) is extremely rare, and the case we report is of a particular site with partial bone destruction. Case presentation: This case report can further strengthen the understanding of EMC and guide clinical treatment. The patient presented with a right buttock mass that was present for 1 year and that had gradually enlarged with tenderness for 6 months. The diagnosis was EMC. The interventions included puncture biopsy, surgical resection, and postoperative chemotherapy. The tumor was resected extensively, and the postoperative recovery was satisfactory. There was no recurrence or metastasis during the follow-up for 18-month. Case presentation: The case we reported occurred in the pelvic cavity, which has not been previously reported in the literature, and there was partial bone destruction. Complete resection of the tumor was performed, and a satisfactory prognosis was achieved.

Simvastatin inhibits the adipogenesis of bone marrow­derived mesenchymal stem cells through the downregulation of chemerin/CMKLR1 signaling.

Simvastatin is effective in the treatment of osteoporosis, partly through the inhibition of the adipogenesis of bone­marrow derived mesenchymal stem cells (BMSCs). The present study focused on the mechanisms responsible for the inhibitory effects of simvastatin on adipogenesis and examined the effects of simvastatin on the expression of peroxisome proliferator­activated receptor γ (PPARγ), chemerin, chemokine­like receptor 1 (CMKLR1), G protein­coupled receptor 1 (GPR1) and the adipocyte marker gene, adiponectin. BMSCs were isolated from 4­week­old female Sprague­Dawley (SD) rats, and adipogenesis was measured by the absorbance values at 490 nm of Oil Red O dye. The expression of each gene was evaluated by western blot analysis or reverse transcription­quantitative PCR (RT­qPCR). The expression of chemerin increased during adipogenesis, while CMKLR1 exhibited a trend towards a decreased expression. On days 7 and 14, the simvastatin­treated cells exhibited a downregulated expression of chemerin, whereas the upregulated expression of its receptor, CMKLR1 was observed. The results also revealed that CMKLR1 is required for adipogenesis and the simvastatin­mediated inhibitory effect on adipogenesis. Simvastatin regulated adipogenesis by negatively modulating chemerin­CMKLR1 signaling. Importantly, simvastatin stimulation inhibited the upregulation of PPARγ and PPARγ­mediated chemerin expression to prevent adipogenesis. Treatment with the PPARγ agonist, rosiglitazone, partially reversed the negative regulatory effects of simvastatin. On the whole, the findings of the present study demonstrate that simvastatin inhibits the adipogenesis of BMSCs through the downregulation of PPARγ and subsequently prevents the PPARγ­mediated induction of chemerin/CMKLR1 signaling.

Association of ADAMTS4 and ADAMTS5 polymorphisms with musculoskeletal degenerative diseases: a systematic review and meta-analysis.

OBJECTIVE: This meta-analysis and systematic review was performed with the aim of investigating the association between a disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)4, AMDMTS5 polymorphisms and risk of musculoskeletal degenerative diseases. METHODS: PubMed, EMBASE, ISI Web of Science, Wanfang and CNKI were searched from their inception until May 2018 to identify eligible studies. Data from individual studies were extracted using a standardized data collection sheet. The estimate of association between ADAMTS4, AMDMTS5 polymorphisms and risk of musculoskeletal degenerative diseases was expressed as odds ratio (OR) along with its related 95% confidence interval (95%CI) under an allelic model of inheritance. Meta-analysis was conducted using RevMan 5.3 software. Subgroup-analyses by ethnicity and type of diseases were performed. RESULTS: Eight studies including ten cohorts were included in this meta-analysis. The meta-analyses results based on seven studies showed that rs226794 in ADAMTS5 gene was not associated with risk of musculoskeletal degenerative diseases (A vs. G: OR 1.07; 95%CI 0.97-1.19; P=0.16). Rs2830585 in ADAMTS5 was significantly associated with musculoskeletal degenerative diseases in only Asians (OR 1.41, 95%CI 1.18-1.68; P=0.0001), but not in Caucasians. Since only two of the collected studies referred to ADAMTS4, we did not perform meta-analysis for these comparisons. CONCLUSION: Taken together, rs226794 and rs2830585 in ADAMTS5 gene were not associated with musculoskeletal degenerative diseases in overall population, but there seemed to be an ethnicity-dependent effect of rs2830585 in the risk of musculoskeletal degenerative diseases. Insufficient evidence was found to support the association of other single nucleotide polymorphisms and musculoskeletal degenerative diseases.