Osteosarcoma has been the most common malignant bone tumor in children and adolescents, while the 5‐y survival of osteosarcoma patients gained no significant improvement over the past decades. This study aimed to explore the role of ferroptosis‐related genes (FRGs) in the development and prognosis of osteosarcoma. The datasets of osteosarcoma patients including RNA sequencing data and clinical information were acquired from the TRGET and Gene Expression Omnibus (GEO) databases. The identification of molecular subgroups with different FRG expression patterns was achieved through nonnegative matrix factorization (NMF) clustering. The prognostic model was constructed using the least absolute shrinkage and selection operator (LASSO) algorithm and multivariate Cox regression analysis. The ESTIMATE algorithm was applied for determining the stromal score, immune score, ESTIMA score, and tumor purity of osteosarcoma patients. Functional analyses including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, Gene Set Enrichment Analysis (GSEA), and Gene Set Variation Analysis (GSVA) were conducted to explore the underlying mechanisms in the development and prognosis of osteosarcoma. Two molecular subgroups with different FRGs expression patterns were identified. The molecular subgroups with higher immune score and more active immune status showed better prognostic survival. On the basis of FRGs, a prognostic model and a nomogram integrating clinical characteristics were constructed and their prediction efficiency for osteosarcoma prognosis were well validated. Gene functional enrichment analysis showed that these differentially expressed FRGs were mainly enriched in immunity‐related signaling pathways, indicating that FRGs may affect the development and prognosis of osteosarcoma by regulating the immune microenvironment. The expression profiles of FRGs were closely related to the immunity status and prognostic survival of osteosarcoma patients. The interaction between ferroptosis and immunity in the development of osteosarcoma could provide a new insight into the exploration of molecular mechanisms and targeted therapies of osteosarcoma patients.

Despite the brilliant bioactive performance of tantalum as an orthopedic biomaterial verified through laboratory researches and clinical practice in the past decades, scarce evidences about the essential mechanisms of how tantalum contributes to osteogenesis were systematically discussed. Up to now, a few studies have uncovered preliminarily the biological mechanism of tantalum in osteogenic differentiation and osteogenesis; it is of great necessity to map out the panorama through which tantalum contributes to new bone formation. This minireview summarized current advances to demonstrate the probable signaling pathways and underlying molecular cascades through which tantalum orchestrates osteogenesis, which mainly contain Wnt/β‐catenin signaling pathway, BMP signaling pathway, TGF‐β signaling pathway, and integrin signaling pathway. Limits of subsistent studies and further work are also discussed, providing a novel vision for the study and application of tantalum.

Objective: To search, review, and analyze the efficacy and safety of various anticoagulants from randomized clinical trials (RCTs) of anticoagulants for THA and TKA. Design: PRISMA-compliant Bayesian Network Meta-analysis. Data sources and study selection: The databases of The Medline, Embase, ClinicalTrial, and Cochrane Library databases were searched until March 2017 for RCTs of patients undergoing a THA or TKA. Main outcomes and measures: The primary efficacy measurement was the venous thromboembolism Odds ratio (OR). The safety measurement was the odds ratio of major or clinically relevant bleeding. OR with 95% credibility intervals (95%CrIs) were calculated. Findings were interpreted as associations when the 95%CrIs excluded the null value. Results: Thirty-five RCTs (53787 patients; mean age range, mostly 55–70 years; mean weight range, mostly 55–90 kg; and a higher mean proportion of women than men, around 60%) included the following Anticoagulants categories: fondaparinux, edoxaban, rivaroxaban, apixaban, dabigatran, low-molecular-weight heparin, ximelagatran, aspirin, warfarin. Anticoagulants were ranked for effectiveness as follows: fondaparinux (88.89% ± 10.90%), edoxaban (85.87% ± 13.34%), rivaroxaban (86.08% ± 10.23%), apixaban (68.26% ± 10.82%), dabigatran (41.63% ± 12.26%), low-molecular-weight heparin (41.03% ± 9.60%), ximelagatran (37.81% ± 15.87%), aspirin (35.62% ± 20.60%), warfarin (9.89% ± 9.07%), and placebo (4.56% ± 6.37%). Ranking based on clinically relevant bleeding events was as follows: fondaparinux (14.53% ± 15.25%), ximelagatran (18.93% ± 17.49%), rivaroxaban (23.86% ± 15.14%), dabigatran (28.30% ± 14.18%), edoxaban (38.76% ± 24.25%), low-molecular-weight heparin (53.28% ± 8.40%), apixaban (71.81% ± 10.92%), placebo (76.26% ± 14.61%), aspirin (86.32% ± 25.74%), and warfarin (87.95% ± 11.27%). No statistically significant heterogeneity was observed between trials. Conclusions and relevance: According to our results, all anticoagulant drugs showed some effectiveness for VTE prophylaxis. Our ranking indicated that fondaparinux and rivaroxaban were safer and more effective than other anticoagulant drugs for patients undergoing THA or TKA.

Osteosarcoma (OS) is the most common malignant tumor of bone. It has recently been demonstrated that galectin-3, a multifunctional β-galactoside-binding, is significantly upregulated in OS tissues, and is correlated with its progression and metastasis. However, the detailed role of galectin‑3 in the regulation of cellular biological processes in OS cells has remained to be elucidated. The present study reported that the mRNA and protein levels of galectin‑3 were significantly increased in OS tissues compared to those in their matched normal adjacent tissues. Furthermore, galectin‑3 was upregulated in three OS cell lines, Saos‑2, MG63 and U2OS, when compared with that in the human osteoblast cell line hFOB1.19. Knockdown of galectin‑3 by galectin‑3‑specific small interfering RNA markedly inhibited OS‑cell proliferation and induced cell apoptosis. Furthermore, silencing of galectin‑3 expression significantly inhibited OS cell migration and invasion, accompanied with a marked decrease in the protein expression of matrix metalloproteinase 2 and ‑9. Mechanistic investigation suggested that the mitogen‑activated protein kinase kinase/extracellular signal‑regulated protein kinase signaling pathway may be involved in the galectin‑3‑mediated OS cell invasion. In conclusion, the present study was the first to report that silencing of galectin‑3 inhibited the malignant phenotypes of osteosarcoma in vitro. Therefore, galectin-3 may serve as a potential therapeutic target for OS.