Prescreening for osteoporosis with forearm bone densitometry in health examination population.

BACKGROUND: Early detection and timely prophylaxis can retard the progression of osteoporosis. The purpose of this study was to determine the validity of peripheral Dual Energy X-ray Absorptiometry (DXA) test for osteoporosis screening. We examined peripheral bone mineral density (BMD) using AKDX-09 W-I DXA densitometer. Firstly, we acquired BMD data from manufacturer-supplied density-gradient phantoms and 30 volunteers to investigate its accuracy and precision, then we measured BMD for 150 volunteers using both AKDX (left forearm) and Hologic Discovery Wi (left forearm, left hip and L1 - L4 vertebrae) simultaneously. Correlation relationship of BMD results acquired from two instruments was assessed by simple linear regression analysis, the Receiver Operating Characteristic (ROC) curves and Areas Under the Curves (AUCs) were evaluated for the diagnostic value of left forearm BMD measured by AKDX in detecting osteoporosis. RESULTS: In vitro precision errors of AKDX BMD were 0.40, 0.20, 0.19%, respectively, on low-, medium-, and high-density phantom; in vivo precision was 1.65%. Positive correlation was observed between BMD measured by AKDX and Hologic at the forearm (r = 0.670), L1-L4 (r = 0.430, femoral neck (r = 0.449), and total hip (r = 0.559). With Hologic measured T-score as the gold standard, the sensitivity of AKDX T-score < - 1 for identifying suboptimal bone health was 63.0 and 76.1%, respectively, at the distal one-third radius and at any site, and the specificity was 73.9 and 90.0%, respectively; the AUCs were 0.708 and 0.879. The sensitivity of AKDX T-score ≤ - 2.5 for identifying osteoporosis at the distal one-third radius and at any site was 76.9 and70.4%, respectively, and the specificity was 80.4 and 78.0%, respectively; the AUCs were 0.823 and 0.778. CONCLUSIONS: Peripheral DXA appears to be a reliable tool for prescreening for osteoporosis.

Trachea repair using an autologous pericardial patch combined with a 3D carbon fiber stent: A case report.

This study is the first to use an autologous pericardial patch combined with a 3D carbon fiber stent for the plastic repair of a large trachea defect. Radical surgery is the optimal therapy for primary malignant tracheal tumors. Tracheoplasty or repair is required to guarantee trachea integrity and normal ventilation function after tracheal tumor resection. Here, we present a case of plastic repair of the trachea using an autologous pericardial patch and a 3D custom-made carbon fiber stent. A 4 cm trachea defect was successfully repaired after resecting a malignant schwannoma. The postoperative ventilatory function was normal without obvious symptoms of discomfort. Fiberoptic bronchoscopy showed a smooth mucosal surface of the endotracheal wall and patency of the airway. CT scans performed 3 years after surgery showed no recurrence. Therefore, we can conclude that a 3D carbon fiber stent is feasible for abolishing patch floating and preventing tracheal stenosis.

Three-dimensional custom-made carbon-fiber prosthesis for sternal reconstruction after sarcoma resection.

Radical resection is the preferred therapy for primary malignant sternal tumors. Sternal reconstruction is required to guarantee the best preservation of respiratory mechanics, and adequate mediastinal protection and acceptable cosmetic results after extensive tumor resection. A wide variety of methods and materials have been described for sternal reconstruction. Titanium implants are preferred by many surgeons because of their optimal features. However, the smooth surface of the metal prostheses does not facilitate the inward growth of the tissue, and the high density of metal can block the X-ray and cause adverse effects on postoperative imaging and radiotherapy. Therefore, in this article we present a case of sternal reconstruction by means of a three dimensional (3D) custom-made carbon-fiber prosthesis following extensive resection of a sternal synovial sarcoma. The microporous structure on the surface of the carbon fiber composite material facilitates the inward growth of the tissue. Low density (1.5 g/cm3 ) of carbon-fiber implant will not block the X-ray and eliminates the adverse effects caused by metal material of postoperative imaging and radiotherapy. The 3D custom-made carbon-fiber prosthesis matched the thoracic defect perfectly and the chest wall reconstruction was stable for more than 24 months.

Nanoparticle-modified chitosan-agarose-gelatin scaffold for sustained release of SDF-1 and BMP-2.

BACKGROUND: Stromal cell-derived factor 1 (SDF-1) is an important chemokine for stem cell mobilization, and plays a critical role in mobilization of mesenchymal stem cells (MSCs). Bone morphogenetic protein 2 (BMP-2) plays a critical role in osteogenesis of MSCs. However, the use of SDF-1 and BMP-2 in bone tissue engineering is limited by their short half-lives and rapid degradation in vitro and in vivo. METHODS: The chitosan oligosaccharide/heparin nanoparticles (CSO/H NPs) were first prepared via self-assembly. Chitosan-agarose-gelatin (CAG) Scaffolds were then synthesized via gelation technology using cross-linked chitosan, agarose, and gelatin, and were modified by CSO/H NPs. The encapsulation efficiency and release kinetics of SDF-1 and BMP-2 were quantified using an enzyme-linked immunosorbent assay. A CCK-8 assays were used to evaluate biocompatibility of NP-modified scaffolds. The biological activity of the loaded SDF-1 and BMP-2 was evaluated using the transwell migration assay and osteogenic induction assay. An animal MSC recruitment model was used to study the ability of SDF-1 released from NP-modified scaffolds to induce migration of MSCs. RESULTS: In this study, we developed a novel nanoparticle-modified CAG scaffold for the delivery of SDF-1 and BMP-2. CCK-8 assays demonstrated excellent biocompatibility of NP-modified scaffolds. In addition, we investigated the release of SDF-1 and BMP-2 from NP-modified scaffolds, and evaluated the effect of released SDF-1 on MSC migration. The effect of released BMP-2 on MSC osteogenesis was also examined. In vitro cell migration assays showed that SDF-1 released from NP-modified scaffolds retained its migration activity; osteogenesis studies demonstrated that released BMP-2 exhibited a strong ability to induce differentiation towards osteoblasts. Our in vivo recruitment assays showed continuous chemotactic response of MSCs to SDF-1 released from the NP-modified scaffold. CONCLUSION: The simplicity of synthesizing CSO/H NP-modified CAG scaffolds, combined with its high cytokine loading capacity and sustained release effect, renders NP-modified CAG scaffold an attractive candidate for sustained release of SDF-1 and BMP-2 to promote bone repair and regeneration.

AKR1B10 promotes breast cancer cell migration and invasion via activation of ERK signaling.

BACKGROUND: Aldo-keto reductase family 1, member B10 (AKR1B10), is known to be significantly induced in the cells of various cancers such as breast cancer. However, the mechanisms of AKR1B10 promoting tumorigenesis in breast cancer remain unclear. In the present study, we demonstrated the potential role and mechanism of AKR1B10 in the invasion and migration of breast cancer cells. METHODS: The expression level of AKR1B10 in breast carcinoma, para-carcinoma and cancer tissues were detected by immunohistochemical evaluation and real-time polymerase chain reaction (RT-PCR), and the correlationships between AKR1B10 expression and clinicopathological features in breast cancer patients (n=131) were investigated. AKR1B10 was ectopically expressed in MCF-7 cells or silenced in BT-20 cells. The roles of AKR1B10 expression in the migration and invasion of MCF-7 cells and BT-20 cells were explored by wound healing assay, transwell migration assay and transwell matrigel invasion assay, and finally the activation level of extracellular signal-regulated kinase 1/2 (EKR1/2) activation and the expression level of matrix metalloproteinase-2 (MMP2) and vimentin in MCF-7 and BT-20 cells were measured by western blot. RESULTS: We found that AKR1B10 expression was increased in malignant tissues, which was correlated positively with tumor size, lymph node metastasis (p<0.05). MCF-7/AKR1B10 cells displayed a higher ability of migration (43.57±1.04%) compared with MCF-7/vector cells (29.12±1.34%) in wound healing assay, and the migrated cell number of MCF-7/AKR1B10 was more (418.43±9.62) than that of MCF-7/vector (222.43±17.75) in transwell migration assay without matrigel. We furtherly confirmed MCF-7/AKR1B10 cells invaded faster compared with MCF-7/vector cells by transwell matrigel invasion assay. Finally, we found AKR1B10 induced the migration and invasion of MCF-7 and BT-20 cells by activating EKR signaling, which promoted the expressions of MMP2 and vimentin. PD98059, a specific inhibitor of the activation of MEK, blocked the migration and invasion by inhibiting the expression of MMP2 and vimentin. CONCLUSIONS: AKR1B10 is overexpressed in breast cancer, and promotes the migration and invasion of MCF-7 and BT-20 cells by activating ERK signaling pathway.

Low expression of Aldo-keto reductase 1B10 is a novel independent prognostic indicator for nasopharyngeal carcinoma.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is one of the most common human head and neck cancers with high incidence in Southern China, Southeast Asia and North Africa. Because of its nonspecific symptoms, the early diagnosis of NPC is very difficult. The 5-year survival rate is not ideal in spite of great innovations in radiation and chemotherapy treatments. Highly sensitive and specific prognostic biomarkers are eager for NPC clinical diagnosis. To find specific target molecules is very important for individualized treatment. Aldo-keto reductase B10 (AKR1B10) is closely related to tumorigenesis and tumor development, and however, its expression level in NPC tissues is not clear. RESULTS: AKR1B10 expression levels were validated in benign, para-cancerous nasopharyngeal and NPC tissues by immunohistochemical evaluation. AKR1B10 was positively expressed in 42 (82.4 %) of 51 benign specimens, and 235 (98.7 %) of 238 para-carcinoma specimens. This percentage was significantly higher than 44.5 % (133/299) in nasopharyngeal carcinoma tissue (p < 0.01). AKR1B10 mRNA quantitative levels detected by real-time quantitative RT-PCR in 90 NPC tissue samples (0.10 ± 0.21) were significantly lower than that in 15 benign tissue samples (1.03 ± 1.12) (p < 0.01). AKR1B10 expression levels in NPC were correlated negatively with T-classification, lymph node metastasis (p < 0.05). We established nasopharyngeal cancer monoclonal cells CNE-2/AKR1B10 with AKR1B10 stable expression and CNE-2/vector cells without AKR1B10 expression by using a modified lentivirus-mediated method, and found that AKR1B10 inhibited the proliferation of CNE-2/AKR1B10 cells by using MTT assay and flow cytometry, and cell migration by in vitro scratch test. CONCLUSION: Taken together, our data suggest that low expression of AKR1B10 is an independent prognostic indicator in nasopharyngeal carcinoma, and that AKR1B10 may be involved in regulating the proliferation and migration of nasopharyngeal cancer cells.