The surgical navigation system has experienced tremendous development over the past decades for minimizing the risks and improving the precision of the surgery. Nowadays, Augmented Reality (AR)-based surgical navigation is a promising technology for clinical applications. In the AR system, virtual and actual reality are mixed, offering real-time, high-quality visualization of an extensive variety of information to the users (Moussa et al., 2012) [1]. For example, virtual anatomical structures such as soft tissues, blood vessels and nerves can be integrated with the real-world scenario in real time. In this study, an AR-based surgical navigation system (AR-SNS) is developed using an optical see-through HMD (head-mounted display), aiming at improving the safety and reliability of the surgery. With the use of this system, including the calibration of instruments, registration, and the calibration of HMD, the 3D virtual critical anatomical structures in the head-mounted display are aligned with the actual structures of patient in real-world scenario during the intra-operative motion tracking process. The accuracy verification experiment demonstrated that the mean distance and angular errors were respectively 0.809±0.05mm and 1.038°±0.05°, which was sufficient to meet the clinical requirements.

The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to participate in the deterioration of many types of cancer. However, the underlying mechanisms of SNHG1-mediating functions in osteosarcoma (OS) have yet to be elucidated. In the present study, our results showed that SNHG1 was upregulated in OS tissues and cell lines, and high SNHG1 expression predicts poor overall survival of OS patients. Knockdown of SNHG1 inhibited cell growth and metastasis of OS in vitro and in vivo. Furthermore, our data demonstrated that there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. Additionally, we identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. Collectively, these findings not only uncovered that the SNHG1/miR-326/NOB1 signaling axis has a key role in OS progression but also suggested the potential application of SNHG1 and miR-326 as biomarkers in the OS diagnosis and treatment.

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This study suggests an intuitive approach for guiding screw placement by way of AR-based navigation. This approach was feasible and accurate. It may serve as a valuable tool for assisting percutaneous sacroiliac screw insertion in live surgery.

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We evaluated the efficacy of vascular endothelial growth factor 165 (VEGF₁₆₅) transgenic bone marrow mesenchymal stem cells (BMSCs) for the repair of early-stage osteonecrosis of the femoral head (ONFH) in mature mongrel dogs. This animal model was surgically established by femoral neck osteotomy and subsequent repinning. Twenty-seven dogs (54 hips) were divided into 3 equal-sized groups: a pCI-neo-VEGF₁₆₅ BMSC group, a pCI-neo BMSC group and a core decompression-alone group. The lipofectamine was used to introduce the VEGF₁₆₅ gene into the BMSCs. After core decompression, transgenic and non-transgenic autologous BMSCs were implanted. Therapeutic efficacy, including new bone formation and neovascularization in the femoral head, was examined by computed radiography, single-photon emission computed tomography, histological and histomorphometric analysis and immunofluorescent staining for von Willebrand factor in pathological sections. The femoral osteotomy site healed completely by the 4th week after the osteotomy surgery and regions of histologically evident osteonecrosis were found 12 weeks later. A regular arrangement of trabeculae and obvious bone regeneration were observed in the animals receiving implanted VEGF-transgenic BMSCs. The quantity of newly generated capillaries was significantly increased in the pCI-neo-VEGF₁₆₅ BMSC group, but there was no significant difference between the pCI-neo BMSC group and the core decompression-alone group. These results demonstrated that VEGF₁₆₅ transgenic autologous BMSCs enhanced bone reconstruction and blood vessel regeneration in the ONFH model. Compared with non-transgenic BMSCs, this approach could provide advanced benefits in the treatment of ONFH.