Non-small-cell lung cancer (NSCLC) is the leading cause of cancer-related death. Developing minimally invasive techniques that can diagnose NSCLC, particularly at an early stage, may improve its outcome. Using microarray platforms, we previously identified 12 microRNAs (miRNAs) the aberrant expressions of which in primary lung tumors are associated with early-stage NSCLC. Here, we extend our previous research by investigating whether the miRNAs could be used as potential plasma biomarkers for NSCLC. We initially validated expressions of the miRNAs in paired lung tumor tissues and plasma specimens from 28 stage I NSCLC patients by real-time quantitative reverse transcription PCR, and then evaluated diagnostic value of the plasma miRNAs in a cohort of 58 NSCLC patients and 29 healthy individuals. The altered miRNA expressions were reproducibly confirmed in the tumor tissues. The miRNAs were stably present and reliably measurable in plasma. Of the 12 miRNAs, five displayed significant concordance of the expression levels in plasma and the corresponding tumor tissues (all r>0.850, all P<0.05). A logistic regression model with the best prediction was defined on the basis of the four genes (miRNA-21, -126, -210, and 486-5p), yielding 86.22% sensitivity and 96.55% specificity in distinguishing NSCLC patients from the healthy controls. Furthermore, the panel of miRNAs produced 73.33% sensitivity and 96.55% specificity in identifying stage I NSCLC patients. In addition, the genes have higher sensitivity (91.67%) in diagnosis of lung adenocarcinomas compared with squamous cell carcinomas (82.35%) (P<0.05). Altered expressions of the miRNAs in plasma would provide potential blood-based biomarkers for NSCLC.

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Background:The SH3 domain of IRSp53 interacts with several proteins that control actin dynamics. Results: IRSp53 interacts with mDia1 and WAVE2 within filopodia, and knocking down either protein reduces IRSp53-driven filopodium formation. Conclusion: IRSp53-mediated filopodium formation involves the actin regulators mDia1 and WAVE2. Significance: Identifying proteins involved in filopodium formation enables an understanding of how these structures arise in mammalian cells.

To facilitate optimal application of appropriate scaffold architectures for clinical trials, there is a need to compare different scaffold modifications under similar experimental conditions. In this study was assessed the effectiveness of poly-e-caprolactone (PCL) scaffolds fabricated by fused deposition modelling (FDM), with varying material modifications, for the purposes of bone tissue engineering. The incorporation of hydroxyapatite (HA) in PCL scaffolds, as well as precalcification through immersion in a simulated body fluid (SBF) to produce a biomimetic apatite coating on the scaffolds, was assessed. A series of in vitro studies spanning 3 weeks as well as in vivo studies utilizing a subcutaneous nude mouse model were carried out. PCL and HA-PCL scaffolds demonstrated increasing tissue growth extending throughout the implants, as well as superior mechanical strength and mineralization, as evidenced by X-ray imaging after 14 weeks in vivo. No significant difference was found between PCL and HA-PCL scaffolds. Precalcification with SBF did not result in increased osteoconductivity and cell proliferation as previously reported. Conversely, tensile forces exerted by tissue sheets bridging adjacent struts of the PCL scaffold caused flaking of the apatite coating that resulted in impaired cell attachment, growth and mineralization. The results suggest that scaffolds fabricated by FDM may have load-bearing applications.