Isolated scaphoid dislocation: A case report and review of literature.

BACKGROUND: Isolated dislocations of the scaphoid are extremely rare types of injuries, commonly associated with severe ligament disruptions, and are occasionally misdiagnosed. Treatment options for dislocations of the scaphoid mainly include closed reduction, with or without internal fixation, and open reduction with ligament repair. CASE SUMMARY: A 59-year-old male worker sustained a twisting trauma of his right wrist, caused by a moving belt while he was operating a machine. When he presented at our emergency department, the patient complained of swelling, tenderness, and restriction of movement of the right wrist. Radiographs confirmed a primary complex partial radial dislocation of the scaphoid and some chip fractures of the capitate and hamate. Closed reduction with K-wire internal fixation was performed with the assistance of arthroscopy, and an excellent prognosis was achieved. CONCLUSION: Arthroscopy-assisted reduction is a minimally invasive method to reduce the dislocated scaphoid and maintain the blood supply.

SND1 promotes the proliferation of osteosarcoma cells by upregulating COX­2/PGE2 expression via activation of NF­κB.

Osteosarcoma is the most frequent primary bone tumor. Staphylococcal nuclease domain­containing 1 (SND1) is a multifunctional protein that plays important roles in tumor development and progression. Overexpression of SND1 has been found in several malignancies, however, its expression and function in osteosarcoma is largely unknown. In the present study, we firstly examined the expression of SND1 in 12 pairs of osteosarcoma and healthy bones by immunoblotting and real time­PCR. The results revealed that osteosarcoma tissues expressed significantly high SND1 mRNA and protein expression compared to normal bone tissues. Next, we stably overexpressed SND1 ORF in MG­63 cells and further defined the biological function of SND1 in osteosarcoma by flow cytometry, cell proliferation and in vivo assays. We found that SND1 overexpression significantly promoted cell proliferation and tumor growth in vitro and in vivo. Furthermore, the non­targeted metabolic profiling, ELISA and luciferase reporter assays were performed on stable overexpressing cells and blood samples to elucidate the underlying mechanisms of SND1­mediated oncogenic features. The results revealed that SND1 increased the production of arachidonic acid PGE2. The serum PGE2 expression level had a significant positive association with the SND1 mRNA expression level in osteosarcoma tissues. The SND1 overexpression­stimulated cell proliferation was enhanced by exogenous addition of PGE2. Additionally, we found that SND1 upregulated PGE2 expression through the NF­κB/cyclooxygenase­2 (COX­2) pathway. In summary, our findings revealed the mechanisms of SND1 involvement in osteosarcoma tumor development, and support the targeting of SND1 as a new anti­tumor strategy for patients with osteosarcoma. In addition, SND1 may act as a potential biomarker of the therapeutic strategies utilizing COX­2 inhibitors.

Numerical Investigation on the Biomechanical Performance of Laparoscopic-Assisted Plate Used for Fixing Pelvic Anterior Ring Fracture.

Because of the minimal soft tissue injury, the laparoscopic-assisted internal fixation is a promising technique in fixing the pelvic anterior ring fracture. The aim of this study was to investigate the biomechanical performance of the laparoscopic-assisted plate by the finite element method. Four kinds of implants were investigated, that is, the laparoscopic-assisted plate (LAP), the percutaneous anterior pelvic bridge (PAPB), the transramus intraosseous screw (TIS), and the open reduction (OR). The stability of the implants was investigated under three loading cases, showing that when the LAP was used, the stress at the fracture site was smaller than that at other parts, while for other implants, the high stress was always around the fracture site. In conclusion, the LAP demonstrated a good biomechanical performance in fixing the pelvic anterior ring fracture and is a promising technique in clinical applications.

Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.

Chemotherapeutic insensitivity remains a major obstacle to osteosarcoma treatment. Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) play an essential role in tumourigenesis. However, the potential biological roles and regulatory mechanisms of novel lncRNAs in response to cisplatin treatment are poorly understood. Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway. Thus, these findings demonstrate that LINC00161 is an essential regulator in cisplatin-induced apoptosis, and the LINC00161-miR-645-IFIT2 signalling axis plays an important role in reducing osteosarcoma chemoresistance.

Microfluidics­based optimization of neuroleukin­mediated regulation of articular chondrocyte proliferation.

Due to the low proliferative and migratory capacities of chondrocytes, cartilage repair remains a challenging clinical problem. Current therapeutic strategies for cartilage repair result in unsatisfactory outcomes. Autologous chondrocyte implantation (ACI) is a cell based therapy that relies on the in vitro expansion of healthy chondrocytes from the patient, during which proliferation­promoting factors are frequently used. Neuroleukin (NLK) is a multifunctional protein that possesses growth factor functions, and its expression has been associated with cartilage development and bone regeneration, however its direct role in chondrocyte proliferation remains to be fully elucidated. In the current study, the role of NLK in chondrocyte proliferation in vitro in addition to its potential to act as an exogenous factor during ACI was investigated. Furthermore, the concentration of NLK for in vitro chondrocyte culture was optimized using a microfluidic device. An NLK concentration of 12.85 ng/ml was observed to provide optimal conditions for the promotion of chondrocyte proliferation. Additionally, NLK stimulation resulted in an increase in type II collagen synthesis by chondrocytes, which is a cartilaginous secretion marker and associated with the phenotype of chondrocytes. Together these data suggest that NLK is able to promote cell proliferation and type II collagen synthesis during in vitro chondrocyte propagation, and thus may serve as an exogenous factor for ACI.

Effects of Incorporating Carboxymethyl Chitosan into PMMA Bone Cement Containing Methotrexate.

Treatment of bone metastases usually includes surgical resection with local filling of methotrexate (MTX) in polymethyl methacrylate (PMMA) cement. We investigated whether incorporating carboxymethyl chitosan (CMCS) in MTX-PMMA cement might overcome disadvantages associated with MTX. To determine the optimal CMCS+MTX concentration to suppress the viability of cancer cells, an integrated microfluidic chip culturing highly metastatic lung cancer cells (H460) was employed. The mechanical properties, microstructure, and MTX release of (CMCS+MTX)-PMMA cement were evaluated respectively by universal mechanical testing machine, scanning electron microscopy (SEM), and incubation in simulated body fluid with subsequent HPLC-MS. Implants of MTX-PMMA and (CMCS+MTX)-PMMA cement were evaluated in vivo in guinea pig femurs over time using spiral computed tomography with three-dimensional image reconstruction, and SEM at 6 months. Viability of H460 cells was significantly lowest after treatment with 57 µg/mL CMCS + 21 µg/mL MTX, which was thus used in subsequent experiments. Incorporation of 1.6% (w/w) CMCS to MTX-PMMA significantly increased the bending modulus, bending strength, and compressive strength by 5, 2.8, and 5.2%, respectively, confirmed by improved microstructural homogeneity. Incorporation of CMCS delayed the time-to-plateau of MTX release by 2 days, but increased the fraction released at the plateau from 3.24% (MTX-PMMA) to 5.34%. Relative to the controls, the (CMCS+MTX)-PMMA implants integrated better with the host bone. SEM revealed pores in the cement of the (CMCS+MTX)-PMMA implants that were not obvious in the controls. In conclusion, incorporation of CMCS in MTX-PMMA appears a feasible and effective modification for improving the anti-tumor properties of MTX-PMMA cement.

An integrated microfluidic device for screening the effective concentration of locally applied tacrolimus for peripheral nerve regeneration.

The effectiveness of tacrolimus (FK506) for the promotion of nerve regeneration is known. However, at present, due to the fact that systemic application may lead to opportunistic infections and tumors, and that the treatment of peripheral nerve injury with systemic immunosuppression is not generally accepted, FK506 has not been widely used for the treatment of simple or peripheral nerve injury. In this study, a pyramid-shaped microfluidic device was designed and fabricated that was able to analyze the effective concentration of locally applied FK506. After testing the effectiveness of the microfluidic device by measuring the fluorescence intensity of fluorescein isothiocyanate-dextran, rat Schwann cells (SCs) were loaded into the device and cultured for 9 days in the presence of different concentrations of FK506. SC proliferation in the presence of FK506 was concentration-dependent between 0 and 2.5±0.003 ng/ml. The proliferation rate reached a maximum at 1.786±0.014 ng/ml, which was statistically significantly different from the proliferation rate at lower FK506 concentrations. There was no statistically significant difference in the proliferation rate between the 1.786 ng/ml group and groups of higher FK506 concentrations. Furthermore, the SCs in the microfluidic device and a 96-well plate continued to proliferate as the culture time increased. No statistically significant differences were identified between the microfluidic device and a 96-well plate with regard to the proliferation rates in each corresponding group. The results obtained in this study demonstrated that the microfluidic device can be used as an excellent platform for the study of drug concentration at the cellular level, and the effective FK506 concentration for local application is 1.786±0.014 ng/ml.

Fabrication and cell affinity of biomimetic structured PLGA/articular cartilage ECM composite scaffold.

An ideal scaffold for cartilage tissue engineering should be biomimetic in not only mechanical property and biochemical composition, but also the morphological structure. In this research, we fabricated a composite scaffold with oriented structure to mimic cartilage physiological morphology, where natural nanofibrous articular cartilage extracellular matrix (ACECM) was used to mimic the biochemical composition, and synthetic PLGA was used to enhance the mechanical strength of ACECM. The composite scaffold has well oriented structure and more than 89% of porosity as well as about 107 µm of average pore diameter. The composite scaffold was compared with ACECM and PLGA scaffolds. Cell proliferation test showed that the number of MSCs in ACECM and composite scaffolds was noticeably bigger than that in PLGA scaffold, which was coincident with results of SEM observation and cell viability staining. The water absorption of ACECM and composite scaffolds were 22.1 and 10.2 times respectively, which was much higher than that of PLGA scaffolds (3.8 times). The compressive modulus of composite scaffold in hydrous status was 1.03 MPa, which was near 10 times higher than that of hydrous ACECM scaffold. The aforementioned results suggested that the composite scaffold has the potential for application in cartilage tissue engineering.